Metastable States of

Here we present new information on the shape evolution of the very neutron-rich ^{92,94}Se nuclei from an isomer-decay spectroscopy experiment at the Radioactive Isotope Beam Factory at RIKEN. High-resolution germanium detectors were used to identify delayed γ rays emitted following the decay of their isomers. New transitions are reported extending the previously known level schemes. The isomeric levels are interpreted as originating from high-K quasineutron states with an oblate deformation of ß∼0.25, with the high-K state in ^{94}Se being metastable and K hindered. Following this, ^{94}Se is the lowest-mass neutron-rich nucleus known to date with such a substantial K hindrance. Furthermore, it is the first observation of an oblate K isomer in a deformed nucleus. This opens up the possibility for a new region of K isomers at low Z and at oblate deformation, involving the same neutron orbitals as the prolate orbitals within the classic Z∼72 deformed hafnium region. From an interpretation of the level scheme guided by theoretical calculations, an oblate deformation is also suggested for the ^{94}Se_{60} ground-state band.

MiR-204 promotes fracture healing via enhancing cell viability of osteoblasts.

OBJECTIVE: To investigate the effects and related mechanisms of miR-204 on fracture healing. MATERIALS AND METHODS: Mouse osteoblastic cell line MC3T3-E1 was used in our experiment. Three groups were established to investigate the potential function between miR-204 and osteoblastic cells: miR-NC group (negative control), miR-204 mimics group (MC3T3-E1 cells transfected with miR-204 mimics) and miR-204 mimics + inhibitor group (MC3T3-E1 cells transfected with miR-204 mimics and inhibitor). After incubation, cell viability, activity of caspase-3, and migration ability of MC3T3-E1 cells, were measured. Further, the expression levels of Runt-related transcription factor 2 (RUNX2) and Osterix (OSX) were detected and analyzed. RESULTS: Compared with miR-NC group, the cell viability and migration ability of MC3T3-E1 cells were enhanced while the activity of caspase-3 was respectively mitigated. Besides, the expression level of RUNX2 and OSX was increased by treatment of miR-204 mimics. However, these variations of the indicators were reversed by the intervention using miR-204 inhibitor. CONCLUSIONS: We revealed the promotion effect of miR-204 on fracture healing, indicating that miR-204 could be a potential therapeutic target for the treatment of a fracture.

[Analysis of vertebrobasilar dolichoectasia based on computational fluid dynamics].

OBJECTIVE: To analyze the hemodynamic states of vertebrobasilar dolichoectasia based on computational fluid dynamics technique. METHODS: The original DICOM format image data from a patient with vertebrobasilar dolichoectasia (VBD), were imported by the Mimics software directly,and the 3D Objects were constructed.The simulation of model was made with Ansys software, the hemodynamic parameters such as streamlines, wall shear stress (WSS) and wall pressure were described. RESULTS: There was stable laminar flow in proximal basilar artery and was no blood flow mixed by bilateral vertebral artery.However, Spiral flows were appeared in distal tortuous basilar artery. The low WSS regions in the vertebrabasilar junction section and inferior segment of basilar artery were coincide with the high wall pressure regions.It could be speculated the initial growth regions might be located in the vertebrabasilar junction section and inferior segment of basilar artery.Local regions with low WSS and high wall pressure might be associated with the occurrence and development of VBD. CONCLUSION: CFD numerical simulation maybe can provide a theoretical basis for the role of hemodynamic factors in occurrence and development of VBD.

Electromagnetic transition rates in 100,101Pd using the Recoil Doppler Shift Technique.

The quadrupole deformations for the low-lying states in the transitional nuclei 100,101Pd have been deduced through the measurement of their electric quadrupole transition probabilities using the Recoil Distance Doppler Shift Method. The nuclei were studied using a 268 MeV 80Se beam impinging on a thin, self-supporting 24Mg target. States in 100Pd and 101Pd populated by the four and three neutron evaporation channels respectively, with reaction gamma-rays detected using the SPEEDY gamma-ray detection array. The recoiling nuclei were stopped in a copper foil and gamma-ray coincidence data taken at 10 separate target-stopper distances between 35 µm and 750 µm. The mean-lifetimes for the lowest lying 2+ (in 100Pd) and 15/2- (in 101Pd) states were measured to be 13.3(9) ps and 10.8(8) ps respectively. These data are compared with predictions from nuclear Total Routhian Surface calculations, which are found to agree with the experimentally deduced values to within 10%.

Role of ALDP (ABCD1) and mitochondria in X-linked adrenoleukodystrophy.

Peroxisomal disorders have been associated with malfunction of peroxisomal metabolic pathways, but the pathogenesis of these disorders is largely unknown. X-linked adrenoleukodystrophy (X-ALD) is associated with elevated levels of very-long-chain fatty acids (VLCFA; C(>22:0)) that have been attributed to reduced peroxisomal VLCFA beta-oxidation activity. Previously, our laboratory and others have reported elevated VLCFA levels and reduced peroxisomal VLCFA beta-oxidation in human and mouse X-ALD fibroblasts. In this study, we found normal levels of peroxisomal VLCFA beta-oxidation in tissues from ALD mice with elevated VLCFA levels. Treatment of ALD mice with pharmacological agents resulted in decreased VLCFA levels without a change in VLCFA beta-oxidation activity. These data indicate that ALDP does not determine the rate of VLCFA beta-oxidation and that VLCFA levels are not determined by the rate of VLCFA beta-oxidation. The rate of peroxisomal VLCFA beta-oxidation in human and mouse fibroblasts in vitro is affected by the rate of mitochondrial long-chain fatty acid beta-oxidation. We hypothesize that ALDP facilitates the interaction between peroxisomes and mitochondria, resulting, when ALDP is deficient in X-ALD, in increased VLCFA accumulation despite normal peroxisomal VLCFA beta-oxidation in ALD mouse tissues. In support of this hypothesis, mitochondrial structural abnormalities were observed in adrenal cortical cells of ALD mice.

Regional expression of Par-4 mRNA and protein after fluid percussion brain injury in the rat.

Regional levels of prostate apoptosis response-4 (Par-4) protein and mRNA were measured after lateral fluid percussion (FP) brain injury in rats. Immunochemical studies indicated that Par-4 immunoreactivity (ir) is present in cortical neurons and hippocampal CA1-CA3 pyramidal neurons in uninjured rats. Increases of Par-4-ir were observed in the CA3 neurons of the ipsilateral hippocampus (IH), but not in injured left cortex (IC) at 48 h after FP brain injury. Levels of the Par-4 mRNA measured by RT-PCR assay and protein measured by Western blot procedure were significantly increased in the injured IC and IH, but not in the contralateral right cortex and hippocampus after brain injury. Levels of both Par-4 protein and mRNA were significantly increased in the IC and IH as early as 2 h and stayed elevated at 24 and 48 h after injury. These data show that the induction of proapoptotic Par-4 mRNA and protein occurs only in the IC and IH that have been observed to undergo apoptosis and neuronal cell loss after lateral FP brain injury. Because increased expression of Par-4 has been observed to contribute to apoptosis and cell death in cultured neurons, the present temporal pattern of Par-4 expression is consistent with a role for Par-4 in apoptosis and neuronal cell death after traumatic brain injury.

Regional expression of Bcl-2 mRNA and mitochondrial cytochrome c release after experimental brain injury in the rat.

Regional levels of anti-apoptotic Bcl-2 mRNA and the cytosolic cytochrome c protein were measured after lateral fluid percussion (FP) brain injury in rats. Levels of Bcl-2 mRNA were significantly decreased in the injured left cortex (IC) and ipsilateral hippocampus (IH), but not in the contralateral right cortex (CC) and hippocampus (CH) after brain injury. Levels of Bcl-2 mRNA were significantly decreased as early as 2 h and stayed decreased as long as 48 h in the IC and IH after injury. Levels of the cytosolic cytochrome c protein were significantly increased in the IC and IH, but not in the CC and CH after brain injury. Levels of cytosolic cytochrome c were significantly increased in the IC at 30 min, 48 and 72 h, and in the IH at 2 h and as long as 72 h after injury. The increase of cytosolic cytochrome c suggests that the mitochondrial release of cytochrome is increased in the IC and IH after lateral FP brain injury. These data show that the reduction of anti-apoptotic Bcl-2 and increases of mitochondrial release of cytochrome c protein occur only in the IC and IH, regions which have been observed to undergo apoptosis and neuronal cell loss after lateral FP brain injury. Therefore, it is likely that the reduction of Bcl-2 and the increased cytochrome c protein in the cytosol contribute to the observed apoptosis and neuronal cell death in the IC and IH after lateral FP brain injury in rats.

[Effects of 3-N-butylphthalide on cortical calcineurin and calpain activities in focal cerebral ischemia rats].

AIM: To explore if the inhibitory effect of 3-n-butylphthalide(NBP) on apoptosis induced by transient focal cerebral ischemia in rats is relevant to cortical calcineurin and calpain activities. METHODS: The model of cerebral ischemia-reperfusion was used. The activities of the two enzymes were measured by using biochemical methods. RESULTS: DL-NBP and D-NBP 20 mg.kg-1 were found to significantly reduce ischemia ipsilateral cortical calcineurin and calpain activities. However, L-NBP 20 mg.kg-1 showed no obvious effect. CONCLUSION: The anti-apoptotic effect of NBP may be relevant to its inhibition of calcineurin and calpain activities in focal cerebral ischemia rats.