Strong-coupling effects in d-wave superconductors.
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Biomedical subjects
Publications and source records attributed to C Jiang.
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Spontaneous nucleosomal DNA fragmentation (SNDF), characteristic of apoptotic cell death was observed in a murine leukemic cell line grown to high density. This effect was eliminated by permitting free diffusional exchange with a large amount of complete medium. Cells seeded at low density did not show SNDF in a conditioned medium that had been used to culture cells with severe SNDF. Cells seeded at high density in the same conditioned medium showed pronounced SNDF, but addition of 10% fetal bovine serum to such a medium significantly reduced SNDF. These observations indicate that neither physical contact among cells in high density culture per se nor secretion of a death factor by the high density culture could account for the induction of SNDF. The results support a model in which the gradual depletion of a serum factor(s) leads to the activation of a cell death program that is manifested as SNDF.
Apparent kinetic parameters have been measured for the transfer of N-acetyl-D-neuraminic acid (Neu5Ac) from CMP-Neu5Ac to analogues of the Gal(beta 1-4)GlcNAc (type II) and Gal(beta 1-3)GlcNAc (type I) substrates by the rat liver Gal(beta 1-4)GlcNAc alpha 2,6-sialyltransferase and the Gal(beta 1-3/4)GlcNAc alpha 2,3-sialyltransferase. In these acceptor analogues, the substituents of the pyranose rings were modified, particularly by deoxygenation, to identify (i) the key polar groups required for efficient transfer and (ii) the substituents that can be removed or modified. A topography including the 6-hydroxyl of the beta Gal and the 2-acetamido of the GlcNAc unit is required for transfer to a terminal type II disaccharide by the alpha 2,6-sialyltransferase. The other hydroxyls can be replaced by hydrogen without a substantial decrease in activity. The alpha 2,3-sialyltransferase requires the 3-, 4-, and 6-hydroxyls of the terminal beta Gal and some contribution from the subterminal sugar. This may explain the cross-reactivity of this enzyme for the type I and type II acceptors. For both enzymes, an influence of the hydrophobic nature of the aglycone is noticed. The results allow an evaluation of the efficiency of the transfer of Neu5Ac to modified substrates.
The effect of hypoxia on ionic currents was studied in acutely dissociated substantia nigra neurons. Using an external solution containing 0 mM Na+ and 0.5 mM Co2+, we found that overall whole-cell outward currents increased by 15-20% during 3-4 min of hypoxia. This current was voltage sensitive and could be completely blocked by TEA- and Cs+, suggesting that this is a K+ current. In cell-attached patches with 150 mM K+ in the external solution, we recorded a large-conductance outward current which was not observed during baseline and was reversibly activated by hypoxia. These results therefore provide the first direct evidence for the activation of K+ channels during O2 deprivation in central neurons.
During their premenopausal years, women have a lower risk than men of getting cardiovascular disease. This protection continues after the menopause if women receive oestrogen replacement. Based on new experimental evidence we propose that some of the cardiovascular benefits of oestrogen replacement therapy may be due to a long-term calcium antagonist effect of oestrogen.
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A model is proposed for the description of effects of safety measures introduced into a road transport system. The model explains the motives of road users' risk compensation towards the measures, and indicates when behavioural adaptation is likely to take place and its effects on road safety programmes. At its core the model has the notion that when a transport system is changed by engineering safety measures, road users do not respond only in the direction towards safety improvement but respond, in general, with three possible ways of behavioural adaptations, one of them towards more risk taking. Supported by illustrative examples, it also suggests that due to risk compensation, engineering safety measures alone are usually not sufficient, and, hopefully, carefully designed motivational safety measures can give us chances to modify road users' behaviour to make traffic safer.
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The liver-specific enhancer of the serum albumin gene contains an essential segment, designated eH, which binds the hepatocyte nuclear factor 3 alpha (HNF3 alpha) and ubiquitous nuclear factor 1/CCAAT transcription factor (NF1/CTF) proteins in tight apposition. We previously showed that activation of transcription by the eH site was correlated with an increase in intracellular HNF3 alpha levels during the in vitro differentiation of the hepatic cell line H2.35. We now show that transfection of an HNF3 alpha cDNA expression vector into dedifferentiated H2.35 cells is sufficient to induce transcription from the eH site. Mutational analysis of the enhancer demonstrates that NF1/CTF cooperates with HNF3 alpha to induce enhancer activity. However, when the eH site is removed from the context of the enhancer, NF1/CTF can inhibit transcriptional activation by HNF3 alpha. We conclude that the ternary complex of HNF3 alpha, NF1/CTF, and the eH site forms a novel, composite regulatory element that is sensitive to the local DNA sequence environment and suggest that the transcriptional stimulatory activity of NF1/CTF depends on its higher-order interactions with other proteins during hepatocyte differentiation.
When the central nervous system in humans is deprived of oxygen, the effects are potentially disastrous. Electroencephalographic activity is lost and higher brain function ceases rapidly. Despite the importance of these effects, the mechanisms underlying the loss of cortical activity are poorly understood. Using intracellular recordings of human neocortical neurons in tissue slices, we show that, whereas anoxia produces a relatively small depolarization and modest alterations in passive properties, it causes a major decrease in excitability. Whole-cell voltage-clamp studies of acutely isolated human neocortical pyramidal neurons demonstrate that anoxia and metabolic inhibition produce a large negative shift in the steady-state inactivation [h infinity (V)] curve for the voltage-dependent sodium current (INa). Inclusion of ATP in the patch pipette decreased the shift of the h infinity (V) curve by two-thirds. Because increased inactivation of INa decreases cellular metabolic demand, we postulate that this promotes neuronal survival during periods of oxygen deprivation. These data show a novel mechanism by which anoxia links metabolism to membrane ionic conductances in human cortical neurons.
By using oligonucleotide-mediated site-directed mutagenesis, we obtained three human interleukin-2 analogs with substitution of Pro in the C-terminal amphiphilic alpha-helix, 125Pro-IL-2, 127Pro-IL-2 and 125Pro-127Pro-IL-2. The bioactivities of all these analogs were decreased. The extent of the decrease in bioactivity coincided with the degrees of secondary and tertiary structure destroyed, as evaluated by circular dichroism and intrinsic fluorescence analysis. The results suggested that the integrity of the hydrophobic face in the C terminal alpha-helix is crucial for the structure and function of interleukin-2.
Polylysine synchronously aggregated pigment granules and egg surface stained uniformly with fluorescein isothiocyanate to form patches (Plate I, fig 1 & 2). Patches always appeared and aggregated first in the opposite grey crescent region, then in grey crescent region and next at animal hemisphere. A fluorescent ring formed at the upper side of the equatorial region. The ring and the patches at the animal hemisphere accumulated to the animal pole to make a cap (Plate I, Fig. 3). Finally the vegetal hemisphere broke due to the contraction of egg surface during aggregation. These indicated that four different domains: opposite grey crescent region, grey crescent region, animal and vegetal hemispheres, were present at the fertilized egg surface. Similar domains also occurred at the unfertilized egg surface as revealed by the same treatment suggesting that the opposite grey crescent region of fertilized egg, which corresponding to the sperm entrance region had existed at the mature egg surface. There were three modes in the early stage of patch formation: (1) the features of granular protrusions did not change greatly (Plate I, Fig. 5-7), (2) the granular protrusions elongated (Plate I, Fig 8-11) and (3) folds radiated from patch (Plate I, Fig. 12, 13). Around each patch new surface membrane arose, which was similar to the nascent membrane of cleavage furrow.(ABSTRACT TRUNCATED AT 250 WORDS)
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Experiments on anesthetized, spinalized rats were conducted to determine the effects of systemic 5-hydroxytryptophan (5-HTP) administration on: (1) spontaneous phrenic nerve activity and (2) evoked phrenic responses to short latency, non-serotonergic synaptic inputs elicited by electrical stimulation of lateral funiculus. 5-HTP augmented spontaneous phrenic activity and allowed expression of a second, longer latency evoked response. Both effects were antagonized by methysergide. Our results suggest that spinal serotonin increases the efficacy of synaptic inputs to phrenic motoneurons.
Synaptic inputs from afferents in the superior laryngeal nerve (SLN) to medullary respiratory neurons (n = 154) in the dorsal respiratory group (DRG), ventral respiratory group (VRG) and the region of the Bötzinger complex (BOT) were studied in anesthetized cats. Single pulse stimulation of the SLN-evoked monosynaptic EPSPs in most inspiratory bulbospinal (I-BS) neurons in the DRG, and disynaptic or oligosynaptic chloride-dependent IPSPs in other I-BS neurons in the DRG and VRG. Stimulation of laryngeal afferents also inhibited oligosynaptically expiratory bulbospinal neurons in the VRG, and all types of respiratory neurons recorded in the BOT region. Oligosynaptic potentials (usually EPSPs) were recorded in inspiratory and expiratory laryngeal motoneurons. These results provide evidence of a processing of SLN-evoked synaptic responses by all tested groups of medullary respiratory neurons. The pathways mediating these synaptic responses are discussed.
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