Electronic structure and properties of superconducting LiTi2O4.
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Biomedical subjects
Publications and source records attributed to J Yu.
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We have studied the mRNA accumulation of pim and myb genes in two interleukin 2- (IL2-)dependent, CTLL-2 and B6.1, and one IL3-dependent, FDC-P2, murine hematopoietic cell lines. To be able to dissociate the IL2 response from the phenomenon of lymphocyte activation, we used cell lines constitutively expressing the high affinity IL2 receptor. Deprivation of IL2 for 16 h led to an accumulation of CTLL-2 cells in G0/G1, and stimulation with IL2 induced a progression in S phase after 10 h. An increased accumulation of pim mRNA was observed in all cases in response to IL2 or IL3. This regulation did not require de novo protein synthesis and was, in CTLL-2 cells, mostly at the transcriptional level. Expression of myb was more complex: in CTLL-2 and FDC-P2 it is high and constitutive, while in B6.1 it is low and induced by IL2. This difference in myb regulation correlates with the higher level of myb expression in immature cells, as only B6.1 is functionally mature. Furthermore, it shows that transcription of myb does not affect the control of the cell cycle by the growth factors IL2 and IL3. These studies demonstrate that pim belongs to the small group of protooncogenes that can be induced during the primary response to growth factors (fos, myc, and myb) and that constitutive expression of myb, at least at the RNA level, is not sufficient to abrogate the growth factor requirement of hematopoietic cell lines.
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Transient acetylcholinesterase (AChE) activity is characteristic of cortical area 17 of the developing laboratory rat during the second and third postnatal weeks of life. This AChE activity is most intense in a band that corresponds to cortical layer IV and the deep part of layer III, but also is found in the outer half of cortical layer I and in layer VI. The morphology of the pattern of the histochemical reaction product indicates that the transient AChE is characteristic of an axonal terminal field. The present report describes results of 3 sets of experiments aimed at determining the source of transient AChE in cortical area 17. First, placement of lesions in portions of the basal forebrain or in the cingulate bundle results in a decrease in the general pattern of AChE throughout occipital cortex and especially in layer I, but the transient bands of AChE in layers III-IV of cortical area 17 are not eliminated. Second, kainic acid or cobalt chloride injections in cortical area 17 result in the loss of many AChE-positive neuronal somata but do not eliminate the transient pattern of AChE in thalamo-recipient layers of cortical area 17. Similarly, treatment of fetuses with mitotic inhibitors that eliminate many of the neurons destined for granular and supragranular layers does not eliminate transient patterns of AChE. Third, lesions that include the lateral geniculate nucleus of the thalamus or geniculocortical projections result in a marked loss of the pattern of AChE in thalamo-recipient layers of cortical area 17, without significant loss in other layers of area 17 or in other regions of occipital cortex. These data support the hypothesis that the transient AChE found in thalamo-recipient layers of cortical area 17 is contained within geniculocortical axon terminals.
Deoxyadenosine plus deoxycoformycin (dCf) causes increased DNA breaks in lymphoid cells. This study explored the possible inhibition of repair synthesis of DNA by dAdo plus dCf as a cause of DNA breakage. It was shown that DNA breaks accumulated in a human T-lymphoblast cell line, CCRF-CEM, following incubation with dAdo plus dCf and were not fully repaired 20 h after their removal. Analysis of the density distribution of radiolabeled DNA on alkaline CsCl gradient showed that incubation of CCRF-CEM cells with dAdo plus dCf caused inhibition of semiconservative, but not repair synthesis of DNA. Semiconservative synthesis of DNA was also inhibited in CCRF-CEM nuclei isolated from cells pretreated with dAdo and dCf, suggesting damage to DNA replicative machinery. However, no such inhibition was observed in the nuclei of a similarly treated CCRF-CEM mutant that was deficient in adenosine kinase and deoxycytidine kinase. This suggests that dAdo must be phosphorylated in intact cells to exert its effect. Using [3H]dTTP incorporation in isolated CCRF-CEM nuclei to measure DNA synthesis, it was found that a high concentration (greater than 100 microM) of dATP inhibits semiconservative but not repair synthesis of DNA. The present studies thus indicate that accumulation of DNA strand breaks induced by dAdo plus dCf is not the consequence of inhibition of repair DNA synthesis. This implies the mechanism may involve perturbation of DNA ligation or activation of a certain process which causes DNA strand breaks. In addition, dATP may interfere with some steps of semiconservative DNA synthesis, but not the repair synthesis of DNA.
Infant albino rats were exposed to a static electromagnetic field of 0.0 Tesla (control) or 0.5 Tesla (experimental) for 14 postnatal days. Following a 1-month rest period, the experimental (13 males and 10 females) and control (11 males and 14 females) rats were trained on four successive reversals of a position habit in a single-unit enclosed T-maze that was adapted for the use of escape-avoidance of mild foot shock as a motive. There was no significant difference in learning ability between the experimental and control groups in terms of total (initial combined with repetitive) errors committed over the four reversal problems. While the females tended to make more errors than the males, this difference was likewise insignificant.
Averaged F-wave conduction velocities (a-FWCV) of peroneal nerve were measured on 38 healthy volunteers and 22 patients with clinical and electromyographic evidence of unilateral L5 or L5 + S1 radiculopathy. The peroneal nerve was stimulated supramaximally at the fibular head and the compound muscle action potential was recorded from the extensor digitorum brevis muscle. Averaged tracings from 32 consecutive stimuli were obtained. The averaged F-wave latency (Fp) and M-wave latency (Mp) were measured from the stimulating artifact to the peak of the waves. The distance (D) between the stimulating point and the T12 spinous process was measured. The value of a-FWCV was calculated as 2D/(Fp-Mp-1) m/second. In normal subjects, the average value of a-FWCV was 56 +/- 4, and there was no significant difference between males and females, nor between the right and left sides. The differences among the tests administered at different times on the same subject were also statistically insignificant. Of the 22 patients, 17 had subnormal value of a-FWCV if the lower normal limits were defined as mean minus 2.5 SD (i.e., 46 m/second) calculated from the normal control value. However, only one of them had subnormal value of FWCV calculated by the conventional method (without averaging technique). All the patients with two root (L5 + S1) involvement had subnormal a-FWCV. It is concluded that the a-FWCV is a more sensitive measure than the conventional FWCV in the assessment of L5 radiculopathy.
The transport of l-[(14)C]glutamine in oat (Avena sativa L.) and spinach (Spinacia oleracea L.) chloroplasts was studied by a conventional single-layer and a newly developed stable double-layer silicone oil filtering system. [(14)C]Glutamine was actively transported into oat chloroplasts against a concentration gradient. Metabolite uptake was greatly affected by the endogenous dicarboxylate pools, which could be easily changed by preloading the chloroplast with specific exogenous substrate. Glutamine uptake was decreased by 44 to 75% in oat chloroplasts preloaded with malate, 2-oxoglutarate (2-OG), and aspartate, but increased by 52% in chloroplasts preloaded with l-glutamate. On the other hand, the uptake of the other four dicarboxylates was decreased by 47 to 79% in chloroplasts preloaded with glutamine. In glutamine-preloaded chloroplasts the uptake of glutamine was inhibited only by l-glutamate. The observed inhibition by l-glutamate was competitive with an apparent K(i) value of 32.1 millimolar in oat and 6.7 millimolar in spinach chloroplasts. This study indicates that there are two components involved in glutamine transport in chloroplasts. The major component was mediated via a specific glutamine translocator. It was specific for glutamine and did not transport other dicarboxylates except l-glutamate. A K(0.5) value of 1.25 millimolar and V(max) of 45.5 micromoles per milligram of chlorophyll per hour were determined for the glutamine translocator in oat chloroplasts. The respective values were 1.0 millimolar and 16.7 micromoles per milligram of chlorophyll per hour in spinach chloroplasts. A three translocator model, involving the glutamine, dicarboxylate, and 2-OG translocators, is proposed for the reassimilation of photorespiratory NH(3) in chloroplasts of C(3) species. In this three-translocator model the additional transport of glutamine into the chloroplast is coupled to the export of glutamate via the glutamine translocator. This is an extension of the two-translocator model, involving the dicarboxylate and 2-OG translocators, proposed for spinach chloroplasts, (KC Woo, UI Flügge, HW Heldt 1987 Plant Physiol 84: 624-632).
The selenium status of children with phenylketonuria on a synthetic low phenylalanine diet was assessed. Correlation between blood selenium and red cell glutathione peroxidase was unsatisfactory (r = 0.65) due to the poor discrimination of red cell glutathione peroxidase with a low selenium diet. No symptoms of deficiency were observed. Supplementation with 50 micrograms per week of selenium as brewers yeast tablets over a period of 6 months significantly increased the blood selenium of the phenylketonuric children. Plasma Vitamin E levels were within normal limits. The supplementation effectively doubled their selenium intake to 15-17 micrograms per day, which is probably sufficient for this group with an adequate Vitamin E status, though considerably lower than the recommended minimum intake of 50 micrograms per day.
Axillary F-loop latencies (AFLL) were measured on median and ulnar nerves of 54 normal volunteers. The median and ulnar nerves were stimulated at the wrist and at the axilla 25cm distal to the sternal notch. The compound muscle action potentials were recorded from thenar and hypothenar muscles. Averaged tracings from 32 consecutive stimuli at the wrist were obtained. The averaged F-wave latencies were measured to the peak (Fwp) of the averaged F-wave. The M-wave latencies from wrist and axilla stimulation were measured to the onset of the wave (Mw and Ma, respectively). The averaged AFLL (a-AFLL) was calculated as (Fwp + Mw)-2 Ma. The average values of a-AFLL were 14.12 +/- 0.88msec for median nerve, and 13.97 +/- 0.90msec for ulnar nerve. There was no significant difference between male and female subjects, nor between the right and left sides. Seven subjects with EMG evidence of C8 or C8 to T1 radiculopathy, although manifesting normal AFLL gauged by the regular method (ie, measured to the onset of the shortest F-wave latency among eight tracings), had significantly longer "averaged AFLL" in both median and ulnar nerves of the affected side than the a-AFLL obtained from the normal side. It is concluded that the a-AFLL is a more sensitive measure than the "regular AFLL" in the assessment of proximal nerve lesion (especially C8 or C8 to T1 radiculopathy).
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Bilateral tibial nerves of 18 albino rats were mechanically compressed between knee and ankle. Beginning on the fifth day after compression, ultrasound thermotherapy of 0.5 or 1.0watt/cm2 was applied over the area of nerve compression in one limb for one minute three times per week. The other side (control) was not treated. Motor distal latency (DL), motor nerve conduction velocity (NCV) of the segment with nerve compression, and amplitude of the evoked compound muscle action potential (ACMAP) were measured before and immediately after nerve compression and two or three times per week after compression. The recovery rates of NCV and ACMAP of the tibial nerve treated with ultrasound of 0.5watt/cm2 were significantly faster than those of the control nerve. There was no significant change in the recovery rate of DL. However, if ultrasound of 1.0watt/cm2 was applied, the recovery rate of ACMAP of the treated nerve was slower than that of the control nerve. There were no significant changes in the recovery rates of DL and NCV. Low doses of ultrasound thermotherapy may facilitate recovery of compression neuropathy, but higher doses may induce an adverse effect.
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Using a combination of gel permeation chromatography and freeze fracture electron microscopy it was found that the ability of sulfatides to promote contact activation in human plasma is associated with the ability of sulfatides to form bilayer structures. When sulfatides were dispersed in buffer at 70 degrees C by vortexing, large liposomes were found ranging in size between 2-5 micron diameter. Contact activation promoting activity was associated with these particles. Sonication resulted in the formation of small vesicles and stacked vesicles of 400-2000 A diameter and biological activity was associated with these vesicles. Homogeneous preparations of small unilamellar vesicles (500 A diameter) can be obtained by chromatography over Sepharose 2B.
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In the present study cultured astrocytes were implanted into the inferior colliculus of rats to create an astrocyte-enriched field that could be examined autoradiographically. The presence of the astrocytes was confirmed with anti-glial fibrillary acidic protein (GFA) immunocytochemistry. We report the presence of a chloride-dependent glutamate binding site on the implanted astrocytes. In the presence of chloride, the specific glutamate binding detected in the implant area was 5-fold greater than that found in a corresponding contralateral region. When the chloride was replaced with acetate, glutamate binding to the astrocytes decreased by more than 80%. The chloride-dependent binding to the astrocytes was insensitive to inhibition by kainic acid (KA) and N-methyl-D-aspartate (NMDA) and sensitive to quisqualate, L-aspartate, L-2-amino-4-phosphonobutyrate, and L-alpha-aminoadipate. The pharmacology of the binding was very similar to that of the in vitro glutamate binding to membranes from cultured astrocytes and to that of a chloride-dependent transport system identified in a glioma cell line. We conclude that the interaction of glutamate with astrocytes is an important component of the total glutamate binding observed in brain slices.
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