From Ultrafast Photoinduced Small Polarons to Cooperative and Macroscopic Charge-Transfer Phase Transition.

We study by femtosecond infrared spectroscopy the ultrafast and persistent photoinduced phase transition of the Rb0.94Mn0.94Co0.06[Fe(CN)6]0.98 ⋅ 0.2H2O material, induced at room temperature by a single laser shot. This system exhibits a charge-transfer based phase transition with a 75 K wide thermal hysteresis, centred at room temperature, from the low temperature Mn3+-N-C-Fe2+ tetragonal phase to the high temperature Mn2+-N-C-Fe3+ cubic phase. At room temperature, the photoinduced phase transition is persistent. However, the out-of-equilibrium dynamics leading to this phase is multi-scale. Femtosecond infrared spectroscopy, particularly sensitive to local reorganizations through the evolution of the frequency of the N-C vibration modes with the different characteristic electronic states, reveals that at low laser fluence and on short time scale, the photoexcitation of the Mn3+-N-C-Fe2+ phase creates small charge-transfer polarons [Mn2+-N-C-Fe3+]* within ≃250 fs. The local trapping of photoinduced intermetallic charge-transfer is characterized by the appearance of a polaronic infrared band, due to the surrounding Mn2+-N-C-Fe2+ species. Above a threshold fluence, when a critical fraction of small CT-polarons is reached, the macroscopic phase transition to the persistent Mn2+-N-C-Fe3+ cubic phase occurs within ≃ 100 ps. This non-linear photo-response results from elastic cooperativity, intrinsic to a switchable lattice and reminiscent of a feedback mechanism.

Strain wave pathway to semiconductor-to-metal transition revealed by time-resolved X-ray powder diffraction.

One of the main challenges in ultrafast material science is to trigger phase transitions with short pulses of light. Here we show how strain waves, launched by electronic and structural precursor phenomena, determine a coherent macroscopic transformation pathway for the semiconducting-to-metal transition in bistable Ti3O5 nanocrystals. Employing femtosecond powder X-ray diffraction, we measure the lattice deformation in the phase transition as a function of time. We monitor the early intra-cell distortion around the light absorbing metal dimer and the long range deformations governed by acoustic waves propagating from the laser-exposed Ti3O5 surface. We developed a simplified elastic model demonstrating that picosecond switching in nanocrystals happens concomitantly with the propagating acoustic wavefront, several decades faster than thermal processes governed by heat diffusion.

Ultrafast time domain demonstration of bulk magnetization precession at zero magnetic field ferromagnetic resonance induced by terahertz magnetic field.

We report the first observation of sub-terahertz bulk-magnetization precession, using terahertz time-domain spectroscopy. The magnetization precession in gallium-substituted epsilon-iron oxide nano-ferromagnets under zero magnetic field is induced by the impulsive magnetic field of the THz wave through the gyromagnetic effect. Just at the resonance frequency, the linear to circular polarized wave conversion is realized. This is understood as the free induction decay signal radiated from a rotating magnetic dipole corresponding to the natural resonance. Furthermore, this demonstration reveals that the series of gallium-substituted epsilon-iron oxide nano-ferromagnets is very prospective for magneto-optic devices, which work at room temperature without external magnetic field, in next-generation wireless communication.

Photoinduced charge-transfer process in rubidium manganese hexacyanoferrate probed by Raman spectroscopy.

The photoinduced charge-transfer process in Rb(0.94)Mn[Fe(CN)(6)](0.98).0.2H(2)O is investigated by observing the valence states of the metal ions by Raman spectroscopy. The sample in the high-temperature phase is irradiated at the ligand to metal, CN(-)-->Fe(III) and charge-transfer band (lambda=395 nm). The Fe(III)-CN-Mn(II) pair valence state corresponding to the high-temperature configuration is totally depleted after prolonged irradiation, and the Fe(II)-CN-Mn(III) pair valence state corresponding to the low-temperature configuration appears. In addition, two kinds of CN stretching modes, ascribed to Fe(II)-CN-Mn(II) and Fe(III)-CN-Mn(III) pair valence states, are found. The photoproduction process of each pair valence states is well reproduced by a kinetic model assuming a charge transfer from Mn(II) to Fe(III). During irradiation, continuous shifts of the Raman peaks are found and ascribed to a release of the strain due to the lattice mismatching between the high-temperature and the photoinduced phases. This behavior indicates that the photoinduced phase created locally in the high-temperature-phase lattice grows up to a photoinduced phase domain. The conversion efficiency is lowered with decreasing temperature, indicating the existence of an energy barrier. We propose a model, which can explain the existence of an energy barrier in the electronic excited state.

Photo-induced magnetization and first-principles calculations of a two-dimensional cyanide-bridged Co-W bimetal assembly.

A two-dimensional cyanide-bridged Co-W bimetal assembly, (H5O2+)[Co(4-bromopyridine)2{W(CN)8}], was prepared. A synchrotron radiation (SR) X-ray single-crystal measurement shows that the crystal structure is monoclinic in the P21/c space group. Magnetic and spectroscopic measurements show that this assembly takes Co(S = 0)-WIV(S = 0) in the temperature range of 2-390 K. Such a wide temperature range Co-WIV phase has not been reported so far. First-principles calculations show that the band gap is composed of a WIV valence band and a CoIII conduction band. 785 nm light irradiation causes photo-induced magnetization with a Curie temperature of 27 K and a coercive field of 2000 Oe. The crystal structure of the photo-induced phase was determined to have larger lattice constants in the two-dimensional layer (bc-plane) by 3% compared to the original phase, which is due to the expansion of the distance of Co-N. The photo-induced phase returns to the original phase upon thermal treatment. First-principles calculations, and magnetic, and optical measurements prove that this photomagnetism is caused by the optical charge-transfer-induced spin transition from Co(S = 0)-WIV(S = 0) to Co(S = 3/2)-WV(S = 1/2).

Magnetic and Mössbauer investigation of the photomagnetic Prussian blue analogue Na(0.32)Co[Fe(CN)6](0.74).3.4H2O: cooperative relaxation of the thermally quenched state.

Thanks to thermal quenching we investigated the relaxation of the metastable state of Na(0.32)Co[Fe(CN)6](0.74).3.4H2O at low temperature. A self-accelerated process has been observed in agreement with the cooperative character of the system, responsible for the large thermal hysteresis of the charge-transfer-induced spin transition. The mean-field analysis of the relaxation is discussed with respect to the equilibrium properties. A sizable deviation from mean-field behavior is observed at the beginning of the relaxation process, which might be attributed to a preliminary structural relaxation of the quenched state.

Molecular structure of the Japanese hepatitis C viral genome.

The amino acid sequence of the polyprotein deduced from the nucleotide sequence of the Japanese hepatitis C virus genome (N. Kato et al. (1990) Proc. Natl. Acad. Sci. USA 87, 9524-9528) indicated that this virus is a member of a new class of positive-stranded RNA viruses. Several domains of this polyprotein also showed weak homology with those of flaviviruses and pestiviruses including the chymotrypsin-like serine proteinase, NTPase and RNA-dependent RNA polymerase.

Marked sequence diversity in the putative envelope proteins of hepatitis C viruses.

The nucleotide sequences of cDNAs (414 base pairs) encoding parts of putative envelope proteins (gp35 and gp70) of 40 isolates of hepatitis C virus (HCV-J) derived from 30 independent plasma or liver specimens from Japanese patients (13 with chronic hepatitis, 14 with hepatocellular carcinoma and 3 hemophiliacs who had received imported clotting factors), were analyzed using the polymerase chain reaction. Approximately 29-38% of the nucleotide sequences of the HCV-J isolates examined differed from those of isolates from the United States (HCV-US). Furthermore, 12-24% and 8-17% sequence diversities were found within the isolates of HCV-J and HCV-US, respectively. The diversities of the amino acid sequences were the same or greater than those of the nucleotide sequences. We confirmed that two hypervariable regions (HVR1 and HVR2) were present in this amplified region, as described in our previous report (Hijikata et al., 1991a) and we found that the HVR1 regions of HCV-J and HCV-US were 27 and 21 amino acids in length, respectively, and began from the N-terminal amino acid of gp70. HVR2 was found in HCV-J, but not in HCV-US isolates, in which the corresponding region of the genome was conserved. During the analysis, plural HCV genomes were found in 6 of 30 specimens. These plural HCV genomes in a single specimen were concluded to be derived from the same HCV ancestor, because of their relative low sequence diversities (about 10% in their nucleotide sequences).(ABSTRACT TRUNCATED AT 250 WORDS)

Sequence analysis of the proximal promoter region of the human alpha-fetoprotein gene in hepatocellular carcinoma.

We have examined whether or not mutations exist in the proximal promoter region of the human alpha-fetoprotein (AFP) gene in the hepatocellular carcinoma (HCC) tissue. Genomic DNA was extracted from four patients: one HCC tissue, one HCC and its corresponding non-cancerous (cirrhosis) tissues, one liver cirrhosis (LC) tissue without HCC and one matching HCC tissue and peripheral blood leukocytes. Serum concentrations of AFP in the patients ranged from less than 5 to 10,138 ng/ml. Nucleotide sequence was determined by direct sequencing using a single-stranded DNA template that was produced first through the polymerase chain reaction (PCR) amplification and then asymmetric PCR. In one HCC tissue taken from the patient with a high concentration of serum AFP, nucleotides different from published ones were detected at -120 and -113. These changes, however, probably reflect a DNA polymorphism, because peripheral blood leukocytes of the same patient had the same changes. Including this patient, no mutations in the region from -160 to -10 were detected in the HCC specimens we have examined. These results suggest that the extremely proximal promoter region of the AFP gene where glucocorticoid-responsive element and HNF-1 binding sites exist is not responsible for the re-expression of AFP in HCC.

Synergism between the hbx gene and aflatoxin B-1 in the development of murine liver-cancer.

Infection by hepatitis B virus (HBV) and exposure to dietary aflatoxin B-1 (AFB(1)) have both been implicated by epidemiological studies to be important risk factors in the development of hepatocellular carcinoma (HCC). Our ability to derive transgenic mice which develop liver cancer as a consequence of the expression of a single gene from HBV, the HBx gene, provides an opportunity to use this animal model to test whether AFB(1) can induce p53 mutations, particularly at codon 249, which are frequently detected in HCC and, as a result, act synergistically with HBV to accelerate the manifestation of disease. While AFB(1) significantly shortened the latency of tumor development in the HBx transgenic mice, the tumors did not have p53 mutations. As in tumors from the untreated transgenic mice, the p53 tumor suppressor protein is found bound to the HBx protein and sequestered in the cytoplasmic compartment of the tumor cell. Despite the frequent involvement of ras mutations in mouse tumors, we also have not detected activation of the ms p21 protein in the tumors from the AFB(1)-treated mice. We conclude that although AFB(1) can act as a co-factor with HBx to induce HCC in mice, its mode of action in vivo remains obscure.

Gamma-ray induced hepatocarcinogenesis in p53-deficient mice.

BACKGROUND: Mutations in the p53 gene are frequent genetic alterations in human hepatocellular carcinoma (HCC), but, little is known of the molecular genetic changes that occur during murine hepatocarcinogenesis. MATERIALS AND METHODS: To characterize the properties of constitutive p53 deficiency that contribute to liver tumor development, a total of 168 F1 mice of two different strains (C3H, which are susceptible to hepatocarcinogenesis and MSM [Mus. M. molossinus] with a single null p53 allele) were exposed to a single 3-Gy dose of whole-body gamma-irradiation at 4 weeks of age and observed for a period of 360 days. The genotype of the mice and the p53 spectrum of the tumors were investigated by polymerase chain reaction (PCR) analysis. RESULTS: Thirty-five gamma-ray-induced HCCs were obtained as a result of this experiment. 11 (40%) of the mice with liver tumor were wild-type for p53. All liver tumors examined retained the wild-type p53 allele, indicating that p53 itself may not be a target for radiation-induced alteration. Only two p53-deficient mice in the liver tumor group developed thymic lymphomas. The p53-deficient mice showed no significant differences in the number, size, or growth rate of HCC or in the apparent development of HCC. CONCLUSION: These results indicate that p53 deficiency does not enhance the rate of development or degree of malignancy of radiation-induced HCC in mice but may instead favor the development of multiple primary cancers.

[Measurement of the common carotid arterial flow during parabolic flight in the anesthetized rat].

To measure the blood flow of a common carotid artery (CCA) during parabolic flight in the rat, we developed an animal double hold box (ADHB) made of styrene expanded form for the anesthetized rat to keep the animal at a proper posture in an aircaft. Twelve anesthetized rats weighing 291-342 g were surgically operated to mount a ultrasound flowmeter probe (1 mm size,1RS:Transonic Systems Inc.) around the right CCA and to insert a catheter into the right axillar artery for blood pressure measurement. These animals were held comfortably in ADHBs which were placed on the rack installed in the aircraft (MU-300). A total of 27 parabolic flights was performed and the blood flow was measured accurately in 9 rats. This special animal holding facility is useful for various types of animal experiments in an aircraft.

[Interferon therapy to chronic hepatitis type C for the prevention of hepatocarcinogenesis].

Interferon(IFN) therapy for chronic hepatitis(CH) related by hepatitis C virus is useful for the prevention of the appearance of hepatocellular carcinoma(HCC) by both prospective and retrospective study. IFN could be reduced an activity of necro-inflammatory reaction leading toward the reduction of fibrogenesis. Therefore, IFN treated group had a low potential carcinogenesis of the liver indicating the prevention of HCC from CH type C, even if virological complete remmision(CR) could not be obtained after IFN treatment. Biochemical response(BR) group as well as CR group could be inhibited hepatocarcinogenesis compare with non-IFN treated group. Recently, IFN applied for liver cirrhosis as same concept for the prevention of HCC.

Detection of HBV DNA in non-A, non-B hepatic tissues using the polymerase chain reaction assay.

The polymerase chain reaction (PCR) followed by Southern blotting was used to examine the presence of hepatitis B virus (HBV) DNA in non-cancerous liver tissue specimens from 22 Japanese hepatocellular carcinoma (HCC) patients, who were negative for HBV surface antigen (HBsAg). By Southern blot analysis, HBV DNA was negative in all 22 patients, but it was detected by the PCR in 8 of the 15 patients who were positive for antibodies against HBsAg or HBV core antigen. Seven patients who were negative for those antibodies were also negative for HBV DNA by the PCR. These results suggest that HBV may be involved in the etiology of the liver disease of some patients with what is presently classified as non-A, non-B hepatitis, if they are positive for HBV antibodies.

Sequence diversity of hepatitis C viral genomes.

The nucleotide sequences of cDNAs (275 base-pairs) in the non-structural protein 5 regions of Japanese isolates of hepatitis C virus (HCV-J) from the plasma of 11 patients with non-A, non-B hepatitis and the livers of five patients with hepatocellular carcinoma were analyzed. Approximately 14 to 17% of nucleotide sequences of the HCV-Js examined differed from that of the original isolate in the United States (HCV-US). Furthermore, 2.5 to 11% sequence diversity was found among the HCV-Js. The nucleotide sequences of the HCV-Js showed characteristic common differences from that of HCV-US, although they also showed some random substitutions. Plural HCV-J genomes were found in two of the cDNAs derived from liver specimens, and a deletion of 102 nucleotides was found in the cDNA derived from one plasma specimen. These results suggest that HCV-J is a strain different from the HCV-US and that mutation of the viral genome occurs at as high a frequency as in that of the human immunodeficiency virus.

Serodiagnostic assay of hepatitis C virus infection using viral proteins expressed in Escherichia coli.

Infection with hepatitis C virus (HCV) was analyzed by an enzyme-linked immunosorbent assay based on recombinant viral proteins encoded by regions of the putative viral core, NS3, NS4 and NS5, which were expressed in E. coli. Results showed that 106 of 124 cases (85.5%) of non-A, non-B chronic hepatitis and 43 of 45 cases (95.5%) of hepatocellular carcinoma, negative for HBV marker, were positive for antibodies against at least one of these viral proteins. One of 87 healthy individuals with normal alanine aminotransferase activity was positive for antibody against only the viral core, but was negative for HCV RNA. The serum of one patient with chronic hepatitis was positive for one of these proteins, but negative for HCV RNA. These findings in combination with results on detection of HCV RNA in the sera of patients with non-A, non-B chronic hepatitis indicated that 105 of 124 cases (84.6%) were positive for HCV infection. Sera that were negative for HCV antibodies against all these proteins were also negative for HCV RNA assayed by reverse transcription followed by the polymerase chain reaction. Screening of HCV infection by detecting viral antibodies in circulating blood using all these viral proteins is useful for reducing the number of ambiguous results in screening for viral infection. Thus, this assay system may be useful diagnostic purposes.

Characterization of hypervariable regions in the putative envelope protein of hepatitis C virus.

We previously identified two hypervariable regions [HVR1 (27 amino acids) and HVR2 (7 amino acids)] in the putative envelope glycoprotein (gp70) by comparison of the amino acid sequences of many isolates of the HCV-II genotype. To understand the functional features of these HVRs, using the polymerase chain reaction we analyzed the rate of actual sequence variability in the region including HVR1 and HVR2 of HCV isolated successively at intervals of several months from two patients with chronic C-type hepatitis. In both patients, the amino acid sequence of HVR1, but not HVR2, was found to change dramatically during the observation period (about one amino acid per month). However, no alteration of the amino acid sequence of HVR1 of HCV was observed in a patient in the acute phase of chronic hepatitis. Restriction digestion analysis of sequence diversity showed that a HCV genome with a newly introduced mutation in HVR1 often became the predominant population at the next time of examination. Alterations of amino acids in HVR1 occurred sequentially in the two patients in the chronic phase. These findings suggest that mutations in HVR1 are involved in the mechanism of persistent chronic HCV infection.