Intermediate band solar cell with extreme broadband spectrum quantum efficiency.

We report, for the first time, about an intermediate band solar cell implemented with InAs/AlGaAs quantum dots whose photoresponse expands from 250 to ∼6000 nm. To our knowledge, this is the broadest quantum efficiency reported to date for a solar cell and demonstrates that the intermediate band solar cell is capable of producing photocurrent when illuminated with photons whose energy equals the energy of the lowest band gap. We show experimental evidence indicating that this result is in agreement with the theory of the intermediate band solar cell, according to which the generation recombination between the intermediate band and the valence band makes this photocurrent detectable.

Growth of bulk ß-Ga2O3 crystals from melt without precious-metal crucible by pulling from a cold container.

We report the growth of bulk ß-Ga2O3 crystals based on crystal pulling from a melt using a cold container without employing a precious-metal crucible. Our approach, named oxide crystal growth from cold crucible (OCCC), is a fusion between the skull-melting and Czochralski methods. The absence of an expensive precious-metal crucible makes this a cost-effective crystal growth method, which is a critical factor in the semiconductor industry. An original construction 0.4-0.5 MHz SiC MOSFET transistor generator with power up to 35 kW was used to successfully grow bulk ß-Ga2O3 crystals with diameters up to 46 mm. Also, an original diameter control system by generator frequency change was applied. In this preliminary study, the full width at half maximum of the X-ray rocking curve from the obtained ß-Ga2O3 crystals with diameters ≤ 46 mm was comparable to those of ß-Ga2O3 produced by edge-defined film fed growth. Moreover, as expected, the purity of the obtained crystals was high because only raw material-derived impurities were detected, and contamination from the process, such as insulation and noble metals, was below the detection limit. Our results indicate that the OCCC technique can be used to produce high-purity bulk ß-Ga2O3 single crystalline substrate.

Primary systemic carnitine deficiency is caused by mutations in a gene encoding sodium ion-dependent carnitine transporter.

Primary systemic carnitine deficiency (SCD; OMIM 212140) is an autosomal recessive disorder characterized by progressive cardiomyopathy, skeletal myopathy, hypoglycaemia and hyperammonaemia. SCD has also been linked to sudden infant death syndrome. Membrane-physiological studies have suggested a defect of the carnitine transport system in the plasma membrane in SCD patients and in the mouse model, juvenile visceral steatosis. Although the responsible loci have been mapped in both human and mouse, the underlying gene has not yet been identified. Recently, we cloned and analysed the function of a novel transporter protein termed OCTN2. Our observation that OCTN2 has the ability to transport carnitine in a sodium-dependent manner prompted us to search for mutations in the gene encoding OCTN2, SLC22A5. Initially, we analysed the mouse gene and found a missense mutation in Slc22a5 in jvs mice. Biochemical analysis revealed that this mutation abrogates carnitine transport. Subsequent analysis of the human gene identified four mutations in three SCD pedigrees. Affected individuals in one family were homozygous for the deletion of a 113-bp region containing the start codon. In the second pedigree, the affected individual was shown to be a compound heterozygote for two mutations that cause a frameshift and a premature stop codon, respectively. In an affected individual belonging to a third family, we found a homozygous splice-site mutation also resulting in a premature stop codon. These mutations provide the first evidence that loss of OCTN2 function causes SCD.

High-power laser experiment forming a supercritical collisionless shock in a magnetized uniform plasma at rest.

We present an experimental method to generate quasiperpendicular supercritical magnetized collisionless shocks. In our experiment, ambient nitrogen (N) plasma is at rest and well magnetized, and it has uniform mass density. The plasma is pushed by laser-driven ablation aluminum (Al) plasma. Streaked optical pyrometry and spatially resolved laser collective Thomson scattering clarify structures of plasma density and temperatures, which are compared with one-dimensional particle-in-cell simulations. It is indicated that just after the laser irradiation, the Al plasma is magnetized by a self-generated Biermann battery field, and the plasma slaps the incident N plasma. The compressed external field in the N plasma reflects N ions, leading to counterstreaming magnetized N flows. Namely, we identify the edge of the reflected N ions. Such interacting plasmas form a magnetized collisionless shock.

Quantitative studies on the polarization optical properties of living cells. I. Microphotometric birefringence detection system.

A method of polarization optical analysis is described in which phase retardation attributable to birefringence of a minute area in a microscopic object is determined. The optical system consists of a polarizing microscope with "rectified" strain-free lenses, a photoelectric detector to determine the intensity of the light passing through a minute window located at the image plane of the specimen, and a stage that moves the specimen at appropriate velocities for scanning. The error resulting from any flare of light emerging from outside of the area to be measured is minimized by limiting the illuminated area. The specimen can be observed during the measurement of light intensity by illuminating the whole microscope field at a wavelength different from that of the light used for the measurement. The retardation of the specimen is determined by comparing the specimen and background intensities as functions of the azimuth of a Brace-Köherl compensator. Alternatively, retardation is obtained directly from the light intensity at a fixed compensator angle, using the theory of polarization optics. The basal noise level for the present apparatus is approximately 0.03 nm when measuring birefringence of a 4-micron2 area in 0.1 s, using a X 40, NA 0.65 objective. The noise decreases in inverse proportion to the square root of the area times the duration of measurement.

Quantitative studies on the polarization optical properties of living cells II. The role of microtubules in birefringence of the spindle of the sea urchin egg.

Birefringence of the mitotic apparatus (MA) and its change during mitosis in sea urchin eggs were quantitatively determined using the birefringence detection apparatus reported in the preceding paper (Hiramoto el al., 1981, J. Cell Biol. 89:115-120). The birefringence and the form of the MA are represented by five parameters: peak retardation (delta p), through retardation (delta t), interpolar distance (D1), the distance (D2) between chromosome groups moving toward poles, and the distance (D3) between two retardation peaks. Distributions of birefringence retardation and the coefficient of birefringence in the spindle were quantitatively determined in MAs isolated during metaphase and anaphase. The distribution of microtubules (MTs) contained in the spindle is attributable to the form birefringence caused by regularly arranged MTs. The distribution coincided fairly well with the distribution of MTs in isolated MAs determined by electron microscopy. Under the same assumption, the distribution of MTS in the spindle in living cells during mitosis was determined. The results show that the distribution of MTs and the total amount of polymerized tubulin (MTs) in the spindle change during mitosis, suggesting the assembly and disassembly of MTs as well as the dislocation of MTs during mitosis.

Electroencephalographic Neurofeedback to up-regulate frontal Theta rhythms: Preliminary results.

Retrieval of positive Autobiographical Memory (AM) has been reported to increase positive emotions in healthy population. Evidence suggests that positive AM retrieval tasks are correlated with synchronisation of frontal Theta rhythms (4-8Hz). The present study has developed the Electroencephalography (EEG) based Neurofeedback (NF) protocols to promote voluntary elevation or up-regulation of positive AM retrieval related Theta rhythms over F3, Fz, F4 electrode sites (10-20 System). The protocols were evaluated with a human participant in 10-day NF training. It observed that the average amplitude of observed Theta rhythms in each NF regulation block gradually increased over days of training and most was prominent at Fz electrode site. Furthermore, a larger peak at 6Hz was present in the spectrum of the observed Theta with later trial day suggesting up-regulation of Frontal Midline Theta (FmT) rhythms.

Glutamate reduces secretion of l-serine in astrocytes isolated from stroke-prone spontaneously hypertensive rats.

In the CNS, l-serine (l-Ser) plays an essential role in neuronal survival by evoking a variety of biological responses in glial cells. Initially, we examined whether glutamate, hydrogen peroxide (H(2)O(2)), interleukin-1 (IL-1) beta, and sodium nitroprusside (SNP) induce the secretion of l-Ser in astrocytes isolated from Wistar Kyoto rats (WKY). The secretion of l-Ser was significantly induced with glutamate and SNP in cultured astrocytes. Next, to gain insight into the involvement of l-Ser in glutamate-induced neuroprotection, we compared the secretion of l-Ser in astrocytes isolated from stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive rats, WKY. We also examined the mRNA expression of the enzyme that produces l-Ser, 3-phosphoglycerate dehydrogenase (PHGDH), and a neural amino acid transporter, ASCT1, in the cultured astrocytes. A dose-dependent study of glutamate in astrocytes of SHRSP indicated differences in the secretion of l-Ser, and gene expression of PHGDH and ASCT1, compared with levels in the WKY astrocytes. We demonstrated that both the secretion and the gene expression were significantly attenuated in glutamate-treated astrocytes from SHRSP. Cerebral ischemia in SHRSP induced a massive efflux of glutamate, causing delayed neuronal death in region CA1 of the hippocampus. The results suggest that the attenuated secretion of l-Ser in astrocytes is involved in neuronal vulnerability and survival in SHRSP during the production of glutamate, as the secretion of l-Ser, which is stimulated by glutamate, is closely related to the protective effect against glutamate-mediated neurotoxicity. We conclude that glutamate and SNP up-regulate the secretion of l-Ser in primary astrocytes. Secretion of l-Ser is regulated in astrocytes in response to glutamate and nitric oxide and may correspond to the level of l-Ser needed for neuronal survival during brain insults such as ischemic stroke in SHRSP.

Solitary adrenal metastasis in a patient with sigmoid colon cancer; report of a case.

A 73-year-old man had sigmoidectomy for sigmoid colon cancer in December 2001. Although he was followed regularly with chemotherapy, his serum carcinoembryonic antigen (CEA) increased on August 2002. Abdominal computed tomography and magnetic resonance imaging showed a right adrenal mass and no other abnormality. The preoperative diagnosis was a solitary adrenal metastasis from sigmoid colon cancer; the lesion was removed in September 2002. On pathology, adrenal metastasis was confirmed. Although the patient's serum CEA normalized soon thereafter, 12 months after adrenalectomy, the CEA again increased; the patient had local recurrence of the resected adrenal lesion and liver metastasis. Therefore, the patient was given systemic chemotherapy, but his condition deteriorated, and he died 38 months after adrenalectomy. Adrenal metastasis from colorectal cancer is not unusual; however, a solitary metastasis is rarely found and resected surgically. As surgical treatment of the metastatic lesion could improve patients' prognosis to some extent if it is detected early, the possibility of adrenal metastasis should be kept in mind when colorectal cancer patients are followed.

Genetic and phylogenetic characterization of rabies virus isolates from wildlife and livestock in Paraiba, Brazil.

Thirty-four rabies virus (RV) isolates from foxes (8), insectivore bats (9), cattle (14), sheep (1), a goat (1) and a donkey (1) from Paraiba state, northeastern Brazil, were genetically characterized. Sequences of 890 nts of nucleoprotein (N) genes of these isolates were analyzed and compared with those of other Brazilian isolates characterized earlier. Phylogenetic analysis revealed three genetical lineages of RV co-existing in this region. Each lineage was found to be associated with particular host species and to circulate independently of each other. The first lineage was found in foxes (Dusicyon sp.) and could be discriminated from domestic carnivore isolates from Sao Paulo, Goias and Minas Gerais in the southern and central Brazil. The second lineage was associated with insectivorous bats (Molossus spp.) and differed from vampire bat-associated RV isolates. The third lineage was found in livestock and clustered with vampire bat-associated RV isolates from Sao Paulo, Tocantins, Goias and Matto Grosso. These results indicate that RV of these genetic lineages are cocirculating in the Paraiba state and that livestock in this region are infected with vampire bat-associated RV, suggesting that the vampire bat is the main reservoir of livestock rabies in this region.

In vivo induction of murine cytokine production by carcinoembryonic antigen.

Carcinoembryonic antigen (CEA) may promote experimental metastasis through production of cytokines. The effect of systemic CEA on the production of proinflammatory cytokines was investigated in mice and compared to levels induced by lipopolysaccharide (LPS). Serum concentrations of interleukin (IL)-6 peaked 1 h after an i.v. CEA injection of 40 microg/mouse to 37-54% of the maximal level induced by a 1 microg/mouse injection of LPS in both normal and immunoincompetent mice. The CEA induction of IL-6 was a specific response, because the peptide PELPK (the pentapeptide on CEA that is the ligand for the CEA receptor on Kupffer cells) conjugated to albumin induced 30% of the maximal CEA response for IL-6, whereas the specificity control PELGK-conjugated albumin did not. IL-1alpha and tumor necrosis factor (TNF)-alpha levels after i.v. injection of CEA were only 3-5% of those induced by LPS. The IL-6 responses of mice pretreated with 100 microg/kg genistein were decreased by more than 40%. However, genistein inhibited the TNF-alpha response to LPS by 46% but increased the CEA-induced response by 300%. When murine Kupffer cells were stimulated with LPS or CEA in vitro, LPS increased tyrosine phosphorylation of a Mr 30,000 protein, whereas CEA decreased phosphorylation of a Mr 60,000 protein and did not increase phosphorylation of the Mr 30,000 protein. Thus, i.v. CEA stimulates production of IL-6 and TNF-alpha after binding to Kupffer cells through signal transduction pathways that appear to be different from those stimulated by LPS.

Role of nitric oxide and superoxide anion in elimination of low metastatic human colorectal carcinomas by unstimulated hepatic sinusoidal endothelial cells.

Human colorectal carcinoma (CRC) cell survival for the first 24 h after implantation in the hepatic sinusoid determines its potential to colonize the liver. Nearly 10-fold more highly metastatic CX-1 cells survive within the livers of nude mice 24 h after intrasplenic injection than weakly metastatic clone A cells. Because CRCs contact sinusoidal endothelial cells (SECs) during implantation, we sought to determine whether SECs were more toxic to clone A than to CX-1 cells. When 2 x 10(4) vital dye-labeled CRC cells were added to murine SEC monolayers, more than 30% of clone A cells lost calcein AM fluorescence compared to fewer than 5% of CX-1 cells after 24 h of coculture with SECs. Kupffer cells did not mediate this effect, because neither enriched Kupffer cells nor SECs treated with a Kupffer cell inhibitor altered the SEC-mediated toxic effect to clone A cells. Pretreatment with a nitric oxide synthase inhibitor, N(G)-monomethyl-L-arginine, superoxide dismutase, or dexamethasone, blocked SEC-mediated toxicity to clone A cells, whereas calcium chelation and catalase did not. In addition, clone A cells were more sensitive to a superoxide donor, 3-morpholinosydnonimine N-ethylcarbamide, than were CX-1 cells, and neither cell line was sensitive to sodium nitroprusside, a nitric oxide donor. Thus, unstimulated murine SECs produce reactive oxygen species that are selectively toxic to weakly metastatic clone A cells. This may be a mechanism by which host liver cells eliminate weakly metastatic neoplastic cells.

Cell adhesion activity for murine carcinoma cells of a wheat germ 55-kDa protein with binding affinity for animal extracellular matrix proteins.

A wheat germ 55-kDa protein was isolated by affinity chromatography with Matrigel immobilized on agarose, followed by preparative gel electrophoresis. This Matrigel-binding protein designated as WG-55 had an amino-terminal amino acid sequence which is identical to that of a putative mature form of wheat storage protein Gbl 1. WG-55 reacted with concanavalin A, indicating its glycoprotein nature as expected from the amino acid sequence of Gbl 1. As expected, similarly, WG-55 exhibited RGD-dependent cell adhesion activity for murine carcinoma cells. These data suggest that WG-55 or mature Gbl 1 protein may play a role in plant cell adhesion.

A cluster of lysinuric protein intolerance (LPI) patients in a northern part of Iwate, Japan due to a founder effect. The Mass Screening Group.

Lysinuric protein intolerance is an autosomal recessive disease characterized by defective transport of the dibasic aminoacids. Mutational analysis of LPI patients in the northern part of Japan revealed that six were homozygous for the R410X mutation and two others were compound heterozygotes of R410X and other unknown mutations. In the population epidemiology study in a local cluster in the northern part of Iwate, ten heterozygotes were found in 1190 newborn babies leading to an estimated LPI incidence of 1/57,000. Polymorphism analysis revealed two major alleles, A and B, in intron 8. While the population frequency of allele A was 0.9 and that of allele B was 0.1 in the northern part of Japan the R410X mutations were exclusively on allele B in 31 chromosomes suggesting a founder effect. Genetic analysis in patients revealed strong linkage disequilibrium with D14S283 and TCRA indicating that the R410X mutation occurred before at least 130 generations ago (about 2600 years). The R410X mutation was shown to be useful as a molecular marker for screening LPI patients in the northern part of Japan.

Carcinoembryonic antigen facilitates experimental metastasis through a mechanism that does not involve adhesion to liver cells.

Carcinoembryonic antigen (CEA) injected intravenously into athymic nude mice increases the ability of weakly metastatic human colorectal carcinoma (CRC) cells to colonize liver in an experimental metastasis assay. Since CEA acts as an intercellular adhesion molecule in vitro, several investigators have postulated that this facilitation of experimental metastasis may be mediated through adhesion between CEA on CRC and CEA-binding proteins on Kupffer or other cells lining the hepatic sinusoid. The present work tested this postulate both by intravital fluorescence videomicroscopy in vivo and in adhesion assays in vitro to enriched populations of Kupffer cells and hepatic sinusoidal endothelial cells (SEC). The data indicate that CEA expression does not effect adhesion to enriched Kupffer cells or SEC in vitro. These data suggest that CEA enhances liver colonization through another mechanism, possibly one that involves modulation of the hepatic response to tumor cell implantation.

Implantation of human colorectal carcinoma cells in the liver studied by in vivo fluorescence videomicroscopy.

In vivo fluorescence videomicroscopy (IVFM) was used to analyse the behavior of weakly and highly metastatic human colorectal carcinoma (CRC) cells during implantation in the liver. A highly metastatic human CRC cell line, CX-1, and a weakly metastatic line, Clone A, were double-labeled with rhodamine B isothiocyanate-dextran (Rd-Dx) to locate cells and with calcein AM to assess cell metabolic activity in an experimental metastasis model. Double-labeled CRC cells (2.0 x 10(6)) were injected into the spleens of groups of nude mice and the livers observed by IVFM over the next 72 h. CRC cells were implanted within 30 s after injection into either portal venules or the proximal third of hepatic sinusoids. Approximately 0.5% of CRC cells traversed the liver through portal-central venous shunts and implanted in the lung. The number of CX-1 cells in the liver was similar to that of Clone A cells during the first 12 h. However, more CX-1 cells than Clone A cells remained in the liver at 4 h and were in groups of 8-12 cells whereas only a few, single Clone A cells were detected in the liver at 72 h. Not all Clone A cells are committed to die within 4 h of implantation because cells harvested 4 h after hepatic implantation proliferated normally in vitro when removed from the hepatic microenvironment. Since the stress of mechanical deformation during implantation may cause differences in cell survival, CX-1 and Clone A cells were passed through filters with 8 microM pores in vitro at 10-15 cm of water pressure to recreate the trauma of hepatic implantation. Approximately 50% of both CX-1 and Clone A cells were lysed. Furthermore, both CRC lines remained metabolically active when co-cultivated with liver cells for at least 24 h in vitro. Thus, the difference in metastatic potential between the two CRC lines may reside in their response to the combination of mechanical implantation and subsequent growth in the liver parenchyma.

Decreased expression of c-myc family genes in thymuses from myasthenia gravis patients.

The thymus is a critical organ for the elimination of autoreactive T cells by apoptosis. We studied the expression of apoptosis-associated genes, bcl-xL, bad, caspase-3, and c-myc family genes in myasthenia gravis (MG) thymuses. We observed that the mRNA levels of myc family genes, c-myc and max, were markedly reduced in MG thymuses. These results indicate that c-myc-mediated signaling is abnormal in MG thymuses. The levels of molecules whose expressions are associated with myc, such as STAM, prothymosin-alpha, and NFkappaB, were also analyzed.

Effects of scatter and attenuation correction on quantitative assessment of regional cerebral blood flow with SPECT.

UNLABELLED: Appropriate corrections for scatter and attenuation correction are prerequisites for quantitative SPECT studies. However, in most cerebral SPECT studies, uniform attenuation in the head is assumed, and scatter is usually neglected. This study evaluated the effect of attenuation correction and scatter correction on quantitative values and image contrast. METHODS: Studies were performed in six normal volunteers (ages 22-26 yr) following intravenous 123I-IMP administration using a rotating, dual-head gamma camera. A transmission scan was acquired with a 99mTc rod source (74 MBq) placed at the focus of a symmetrical fanbeam collimator. Data were reconstructed using two attenuation coefficient (mu) maps: quantitative mu map from the transmission scan and a uniform mu map generated by edge detection of the reconstructed images. Narrow and broad beam mu values were used with and without scatter correction, respectively. Scatter was corrected with transmission-dependent convolution subtraction and triple-energy window techniques. Quantitative rCBF images were calculated by the previously validated IMP-autoradiographic technique, and they were compared with those obtained by (15)O-water and PET. SPECT and PET images were registered to MRI studies, and rCBF values were compared in 39 ROIs selected on MRI. RESULTS: Clear differences were observed in rCBF images between the measured and constant mu maps in the lower slices due to the airways and in the higher slices due to increased skull attenuation. However, differences were < 5% in all cerebral tissue regions, thus assumption of uniform mu introduces little bias. The scatter correction was found to increase the image contrast significantly, i.e., rCBF increased by 20%-30% in gray matter and decreased in white matter regions by 10%-20% after scatter correction, increasing gray-to-white ratio to be close to that of PET measurement. The rCBF values from the two scatter correction were not significantly different, but the triple-energy window technique suffered from increased noise. After scatter correction, rCBF values were in good agreement with those measured by PET. CONCLUSION: This study shows little loss in accuracy results from assuming uniform mu map. However, scatter correction is required for the quantitative rCBF values and gray-to-white ratios to approach those of PET.

Noninvasive quantitation of cerebral blood flow using oxygen-15-water and a dual-PET system.

UNLABELLED: Measurement of the arterial input function is essential for quantitative assessment of physiological function in vivo using PET. However, frequent arterial blood sampling is invasive and labor intensive. Recently, a PET system has been developed that consists of two independent PET tomographs for simultaneously scanning the brain and heart, which should avoid the need for arterial blood sampling. The aim of this study was to validate noninvasive quantitation with this system for 15O-labeled compounds. METHODS: Twelve healthy volunteers underwent a series of PET studies after C15O inhalation and intravenous H2(15)O administration using a Headtome-V-Dual tomograph (Shimadzu Corp., Kyoto, Japan). The C15O study provided gated blood-pool images of the heart simultaneously with quantitative static blood-volume images of both the brain and heart. Weighted-integrated H2(15)O sinograms were acquired for estimating rate constant (K1) and distribution-volume (Vd) images in the brain, in addition to single-frame sinograms for estimating autoradiographic cerebral blood flow images. Noninvasive arterial input functions were determined from the heart scanner (left ventricular chamber) according to a previously developed model and compared directly to invasive input functions measured with an on-line beta probe in six subjects. RESULTS: The noninvasive input functions derived from this PET system were in good agreement with those obtained by continuous arterial blood sampling in all six subjects. There was good agreement between quantitative values obtained noninvasively and those using the invasive input function: average autoradiographic regional cerebral blood flow was 0.412 +/- 0.058 and 0.426 +/- 0.062 ml/min/g, K1 of H2(15)O was 0.416 +/- 0.073 and 0.420 +/- 0.067 ml/min/ml and Vd of H2(15)O was 0.800 +/- 0.080 and 0.830 +/- 0.070 ml/ml for the noninvasive and invasive input functions, respectively. In addition to the brain functional parameters, the system also simultaneously provided cardiac function such as regional myocardial blood flow (0.84 +/- 0.19 ml/min/g), left ventricular volume (132 +/- 22 mm at end diastole and 45 +/- 14 ml at end systole) and ejection fraction (66% +/- 5%). CONCLUSION: This PET system allows noninvasive quantitation in both the brain and heart simultaneously without arterial cannulation, and may prove useful in clinical research.

Mutagenicity of metabolites of carcinogenic aminoazo dyes.

The mutagenicity of 8 azo dyes and 6 p-phenylenediamine derivatives, which comprised the metabolites of carcinogenic 4-aminoazobenzene derivatives, was studied on Salmonella typhimurium TA98 and TA100. 4'-Hydroxy-N-methyl-4-aminoazobenzene and its O-sulfate and O-glucuronide, and 3-hydroxy-4-aminoazobenzene were mutagenic on TA98 in the presence of S-9 mix. p-Phenylenediamine and its o-methoxyl derivative were definitely mutagenic on TA98 with the addition of S-9 mix. All metabolites tested were non-mutagenic on TA100, although the mother azo dyes were mutagenic both on TA98 and TA100 in the presence of S-9 mix. These results rule out a possibility that the mutagenicity, at least on TA100 microbes, of carcinogenic 4-aminoazobenzene derivatives may be mediated by any of the ring-hydroxyl or azo reduction metabolites and their conjugates produced from the azo dyes by incubation with S-9 mix.