X-ray absorption fine structure study on residue bromine in carbons with different degrees of graphitization

The structure of bromine residue compounds was investigated by X-ray absorption fine structure (XAFS) in order to interpret where and how bromine is present in carbons with different degrees of graphitization. The residue compounds can be classified into three groups, as obtained from X-ray absorption near edge structure (XANES) spectra and the values of the intramolecular distance r_Br–Br determined by extended X-ray absorption fine structure (EXAFS). In Group I, prepared from the host carbons heat treated at temperatures higher than 1900 °C, bromine exists in the interlayer space of graphite in the form of Br₂ molecules with interaction of the π electrons of graphite. In Group III, from carbon heat treated at 1000 °C, most of the bromine probably reacts with carbon atoms having a dangling bond or functional groups. For Group II, where the host carbons are heat treated at intermediate temperatures, it is likely that bromine exists in undeveloped defects with a unique electronic state.     

Design of Cavities for a Short Pulse Powerful Large Orbit Gyrotron

Designs of cavities for fundamental and high harmonic operation in Large Orbit Gyrotron (LOG) are discussed. The fundamental operation allows one to use beam currents in the range from 200 A to 300 A achieve output power of the order of 9–10 MW at frequency 143.6 GHz. Mode competition calculations show that stable oscillations in the TE^1,4 mode using high beam currents are possible even with the pitch factor 1.3 which is significantly lower than the design value 1.55. For the second harmonic operation, the maximum current used for excitation of the TE^2,4 mode is 60 A and the optimum magnetic field is 7.6 T. A cavity design for fourth harmonic operation using the TE^4,4 mode is also presented.     

Spatiotemporal expression of C-CAM in the rat placenta

We investigated the expression of the immunoglobulin superfamily cell adhesion molecule, C-CAM, in developing and mature rat placenta. By immunohistochemical staining at the light microscopic level, no C-CAM-expression was seen before Day 9 of gestation, when it appeared in the trophoblasts of ectoplacental cones. On Day 10.5, spongiotrophoblasts and invasive trophoblasts around the maternal vessels of the decidua basalis were stained positively. On Day 12.5, C-CAM was detected in the spongiotrophoblasts of the junctional layer, but labyrinth trophoblasts and secondary giant trophoblasts were not stained. On Day 17.5, C-CAM was found only in the labyrinth and lacunae of the junctional layer. At this stage, both the labyrinth cytotrophoblasts of the maternal blood vessels and the endothelial cells of the embryonic capillaries were strongly stained. Placental tissues from gestational Days 12.5 and 17.5 were analyzed by immunoelectron microscopy to determine the location of C-CAM at the subcellular level. On Day 12.5, positive staining of the spongiotrophoblasts was observed, mainly on surface membranes and microvilli between loosely associated cells. On Day 17.5, staining was found primarily on the microvilli of the maternal luminal surfaces of the labyrinth cytotrophoblasts, and both on the luminal surface and in the cytoplasm of endothelial cells of the embryonic vessels. RT-PCR analysis and Southern blotting of the PCR products revealed expression of mRNA species for both of the major isoforms, C-CAM1 and C-CAM2. Immunoblotting analysis of C-CAM isolated from 12.5-day and 14.5-day placentae showed that it appeared as a broad band with an apparent molecular mass of 110-170 kD. In summary, C-CAM was strongly expressed in a specific spatiotemporal pattern in trophoblasts actively involved in formation of the placental tissue, suggesting an important role in placental development. In the mature placenta, C-CAM expression was confined to the trophoblastic and endothelial cells lining the maternal and embryonic vessels, respectively, suggesting important functions in placental physiology.     

Ischemic damage and subsequent proliferation of oligodendrocytes in focal cerebral ischemia

In order to achieve a better understanding of the pathophysiology of ischemic white matter lesions, oligodendrocytic degeneration and subsequent proliferation were examined in the mouse model of middle cerebral artery occlusion. In situ hybridization histochemistry for proteolipid protein messenger RNA was employed as a sensitive and specific marker of oligodendrocytes, and immunohistochemistry for myelin basic protein was used as a compact myelin marker. Immunohistochemistry for microtubule-associated protein 2 and albumin was employed to monitor neuronal degeneration and the breakdown of the blood brain barrier, respectively. In the ischemic core of the caudoputamen, the immunoreactivity for microtubule-associated protein 2 disappeared and massive albumin extravasation occurred several hours after vessel occlusion, while proteolipid protein messenger RNA signals remained relatively strong at this time. The messenger RNA signals began to attenuate 12 h after ischemia and were hardly detectable 24 h after ischemia in the whole ischemic lesion. In situ end-labeling of fragmented DNA showed some cells with proteolipid protein messenger RNAs to have DNA fragmentation at this period. In contrast to proteolipid protein messenger RNA signals, the immunoreactivity for myelin basic protein was detected as long as five days after ischemia. An apparent increase in the cells possessing strong proteolipid protein messenger RNA signals was found five days after ischemia, mainly in the corpus callosum and the cortex bordering the infarcted areas. A double simultaneous procedure with in situ hybridization for proteolipid protein messenger RNA and immunohistochemistry for glial fibrillary acid protein or lectin histochemistry for macrophages/microglia showed proliferating oligodendrocytes to be co-localized with reactive astrocytes and macrophages/microglia. These findings show that oligodendrocytic damage occurred following ischemic neuronal damage and the breakdown of the blood brain barrier, but preceded the breakdown of myelin proteins in the ischemic lesion, that an apoptosis-like process was involved in ischemic oligodendrocytic death, and that surviving oligodendrocytes responded and proliferated in the outer border of the infarcted area.