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Biomedical subjects

X Sun

Publications and source records attributed to X Sun.

At least 523 records · Page 29Linked to original sources
PubMed1993

Multiple functional domains of human transcription factor IIB: distinct interactions with two general transcription factors and RNA polymerase II.

Transcription factor IIB (TFIIB) plays a pivotal role in the formation of transcription-competent initiation complexes. TFIIB was found to interact with the TATA-binding protein, the small subunit of TFIIF, and RNA polymerase II. These interactions require distinct domains in TFIIB. Using the gel mobility-shift assay, it was found that the amino terminus of TFIIB was necessary for the formation of complexes containing RNA polymerase II and TFIIF, whereas the carboxy-terminal domain, which is composed of two imperfect direct repeats and includes a putative amphipathic alpha-helix, was sufficient for the formation of complexes containing the TATA-binding protein and TFIIB (DB complex). Protein-protein interaction analyses demonstrate that the amphipathic alpha-helix in TFIIB is important for the interaction with the TATA-binding protein. Specific residues mapping to the carboxyl terminus of the second direct repeat were found to be crucial for the interaction of TFIIB and RNA polymerase II. The interaction with the small subunit of TFIIF was mapped to the amino terminus of TFIIB, which includes a zinc finger.

Base Sequence↗
PubMed1993

Selective transcriptional augmentation of hepatic gene expression in the rat with Heymann nephritis.

The synthesis of albumin and other hepatic proteins, many regulated as part of the acute phase response, is increased in the nephrotic syndrome. It has been postulated that synthesis of all proteins secreted by the liver is increased by the same mechanism in the nephrotic syndrome. However, the observation that synthesis of some apolipoproteins is not increased suggests that only a specific group of proteins may be similarly regulated in nephrosis. We measured synthesis of albumin and of two acute phase proteins, fibrinogen and alpha 1-acid glycoprotein (alpha 1-AG), in rats with Heymann nephritis (HN), their mRNA concentration in liver, and the rate of transcription of their genes by hepatic nuclei. Albumin and fibrinogen mRNA levels almost doubled in HN, but alpha 1-AG mRNA was unchanged. Ribosomal RNA (28S) concentration and transcription were also increased significantly in HN. Transcription of albumin and fibrinogen also increased twofold, but transcription of alpha 1-AG was unchanged. Fibrinogen and albumin synthesis each increased more than fourfold in HN and correlated with one another. In contrast alpha 1-AG synthesis only increased by 50% and did not correlate with albumin synthesis. Both albumin and alpha 1-AG were lost in the urine of HN, and their plasma concentrations were reduced. Fibrinogen was not lost in the urine and its plasma concentration was significantly increased in HN. Synthesis of a group of proteins including both positive acute phase (fibrinogen) and negative acute phase (albumin) proteins is increased transcriptionally in the nephrotic syndrome. Synthesis of other proteins is increased posttranscriptionally.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute-Phase Proteins↗
PubMed1993

Extrahepatic lipogenesis contributes to hyperlipidemia in the analbuminemic rat.

Hepatic lipid and apolipoprotein synthesis is increased in the nephrotic syndrome. Catabolism of triglyceride-rich lipoproteins is impaired in nephrotic syndrome but not in rats with hereditary analbuminemia (NA), suggesting that lipid synthesis should be increased by analbuminemia in the absence of proteinuria. In this study the rate of cholesterol and fatty acid synthesis in liver and extrahepatic tissue was measured in female NA and control Sprague-Dawley (SD) rats to determine whether lipid synthesis was indeed increased in isolated analbuminemia and to identify the site(s) of increased lipogenesis. We also measured the concentrations of apolipoproteins (apo) AI, B, and E in plasma, as well as the levels of the respective mRNAs in liver. Plasma cholesterol, triglycerides, and apo AI, B, and E were all increased severalfold in the NA rat (P < 0.001). Although liver apolipoprotein mRNA content was significantly increased (P < 0.001) for apo AI (643%), B (273%), and E (299%), 3-hydroxy-3-methylglutaryl-coenzyme A reductase activity in liver microsomes and hepatic cholesterol synthesis were not significantly increased in the NA rats. Hepatic fatty acid synthesis and intestinal cholesterol synthesis were not increased in the NA rats. Surprisingly, intestinal fatty acid synthesis was elevated by 60% (P < 0.01). The NA rats demonstrated approximately fourfold increases in the incorporation of 3H2O into circulating cholesterol and fatty acids (P < 0.001). A 56% increase in the synthesis of total nonsaponifiable lipid was found in the extravisceral carcass (P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Alterations in contractility and intracellular Ca2+ transients in isolated bundles of skeletal muscle fibers from rats with chronic heart failure.

To determine if chronic heart failure (CHF) leads to functional or structural alterations of skeletal muscle, we compared intracellular Ca2+ signaling, contractility, and the rate of fatigue development, together with electron microscopy (EM), in skeletal muscle preparations from rats with myocardial infarction-induced CHF versus sham-operated control rats. Bundles of 100 to 200 cells were dissected from the extensor digitorum longus (EDL) muscle of control (n = 13) and CHF (n = 19) rats and were either loaded with aequorin or fixed for EM. Muscles from CHF rats exhibited depressed tension development compared with control muscles during twitches (1.4 +/- 0.2 versus 2.8 +/- 0.7 g/mm2, P < .05) and maximal tetani (5.3 +/- 1.4 versus 10.7 +/- 2.4 g/mm2, P < .05). Depressed tension in CHF was accompanied by reduced quantitative [Ca2+]i release during twitches (0.7 +/- 0.1 versus 0.4 +/- 0.1 microM, P < .05) and during maximal tetani (1.8 +/- 0.3 versus 0.9 +/- 0.2 microM, P < .05). Skeletal muscle from CHF rats also demonstrated prolonged intracellular Ca2+ transients during twitches and tetani and accelerated fatigue development. EM revealed a lack of cellular atrophy in the CHF rats. In conclusion, EDL skeletal muscle from rats with CHF had intrinsic abnormalities in excitation-contraction coupling unrelated to cellular atrophy. These findings indicate that CHF is a condition accompanied by EDL skeletal muscle dysfunction.

Aequorin↗
PubMed1993

Modulation of kainic acid-induced activity in the mouse spinal cord by the amino terminus of substance P: sensitivity to opioid antagonists.

Behavioral sensitization to kainic acid (KA) in the mouse spinal cord appears to be mediated by the amino (N) terminus of substance P (SP), as potentiation of KA is sensitive to capsaicin, mimicked by SP1-7 but not SP5-11, and blocked by SP1-7 antagonists but not by neurokinin antagonists. As naloxone inhibits some effects of SP1-7, this study examines the role of opioid receptors in the mediation of KA-induced sensitization by the N terminus of SP. All drugs were injected i.t. Behavioral sensitization to repeated injections of KA was inhibited by a large (1 micrograms) dose of naloxone. Pretreatment with either naloxonazine or beta-funaltrexamine, mu-selective opioid antagonists, naltrindole, a delta-selective opioid antagonist, or nor-binaltorphimine, a kappa-selective antagonist, failed to alter the development of sensitization to KA, indicating that this phenomenon is not due to mu, delta, or kappa opioid receptors. The ability of 22.5 pmol of SP1-7 to enhance subsequent KA responses was blocked when coadministered with 0.1 micrograms of naloxone. When administered with KA, naloxone not only failed to reverse the potentiative effect of SP1-7, but further enhanced responses to KA for 2 hr after SP1-7. In contrast to pretreatment with SP1-7, coadministration of KA with SP1-7 inhibited the intensity of behaviors. The inhibitory effect of SP1-7 on responses to a single injection of KA was prevented by pretreatment with naltrindole, whereas pretreatment with beta-funaltrexamine blocked the inhibitory effect of SP1-7 on response to KA in a KA-sensitized animal.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Responses of superior collicular neurons of the big brown bat, Eptesicus fuscus, to stationary and moving sounds.

Responses of 59 superior collicular neurons (SC) of the big brown bat, Eptesicus fuscus, to stationary and moving sounds were studied under free-field stimulation conditions. Neurons responding to sound stimulation were recorded from all three layers of the SC; however, responses of neurons in the superficial and upper intermediate layers generally show poor signal to noise ratio. Spatial sensitivity of each SC neuron was studied by determining variation of the number of impulses and minimum threshold (MT) of the neuron with a sound broadcast from a stationary loudspeaker at several selected azimuthal angles. More than 95% of SC neurons showed a lowest MT and maximal number of impulses to sound broadcast from a contralateral angle. However, the angle of lowest MT and the angle of maximal number of impulses of a given neuron were not always the same. Responses of 40 SC neurons to moving sounds were studied by determining the number of impulses of each neuron to a sound broadcast from a moving loudspeaker at selected azimuthal angles. Most (n = 27, 67%) neurons were sensitive to a sound with low moving velocity (36 degrees/s). There were 9 (23%) neurons which discharged maximally to a sound moved in a preferred direction but poorly when moved in the opposite direction. In addition, 5 (13%) neurons discharged maximally to a sound moving away from the midline and across 20 degrees lateral of the bat's frontal auditory space. These findings suggest that SC neurons may help a bat acoustically "gaze" at insect during hunting.

Acoustic Stimulation↗
PubMed1993

[Application of analytical hierarchy process in the evaluation of quality of management of infectious diseases].

We evaluated the quality of management of infectious diseases in hospitals with analytical hierarchy process (AHP). An attempt to work out assessing model for the management of infectious diseases by establishing a Goal Tree and groups of indices is presented. The rankings, indices and stresses in each assess of this model were established by the request of the content and quality of management of infectious diseases. The Consistent Index (C.I) was used to test whether the contrast rankings of the model were logical, making the logical judgement of evaluated factors quantitated. The results show that the model is scientific and feasible.

China↗
PubMed1993

[The influence of DPDPE on intracellular free calcium concentration induced by Bt2 cAMP and phorbol ester].

The effect of DPDPE on intracellular free calcium concentration in neuroblastoma glioma hybrid cells (NG108-15) was studied with fura-2/AM fluorescence. The results were as follows: 1) The membrane permeable cAMP analogue Bt2cAMP, the adenylate cyclase activator forskolin and the protein kinase C activator TPA all induced an increase in intracellular free calcium concentration. 2) Verapamil suppressed the increase of [Ca2+]i induced by Bt2cAMP, forskolin and TPA. 3) DPDPE blocked the increase of [Ca2+]i induced by Bt2cAMP and forskolin, but not that induced by TPA. These results imply that DPDPE suppresses cyclic AMP-dependent protein kinase-induced but not protein kinase C-induced intracellular free calcium.

Calcium-Transporting ATPases↗
PubMed1993

[Study of patients with spinocerebellar degeneration using positron emission tomography].

We studied cerebral blood flow, oxygen metabolism and their relation to clinical symptoms in 45 patients with spinocerebellar degeneration (SCD) and 12 normal control subjects using positron emission tomography (PET). Regions of interest were acquired for the cerebellar hemispheres, cerebellar vermis, brainstem, thalami, and cerebral cortices. PET studies in these patients revealed that regional cerebral blood flow (CBF), regional cerebral oxygen metabolic rate (CMRO2), CBF/mean CBF of each cerebral cortex (CBF/mCBF) and CMRO2/mean CMRO2 of each cerebral cortex (CMRO2/mCMRO2) in the cerebellar hemispheres, cerebellar vermis, and brainstem showed a significant decrease in comparison with the normal control subjects, while in the cerebral cortices and thalami, SCD patients showed normal values. CBF/mCBF and CMRO2/mCMRO2 were significantly decreased in patients with olivopontocerebellar atrophy (OPCA) and Menzel type of hereditary ataxia (Menzel type) in the cerebellar hemispheres, cerebellar vermis, and brainstem, whereas patients with late cortical cerebellar atrophy (LCCA) and Holmes type of hereditary ataxia (Holmes type) revealed a significant decrease of CBF/mCBF and CMRO2/mCMRO2 in the cerebellar hemispheres and cerebellar vermis, but not in the brainstem. Patients with OPCA showed a significant decrease of CBF in the cerebellar hemispheres, cerebellar vermis, brainstem and that of CMRO2 in the cerebellar hemispheres and cerebellar vermis. Patients with LCCA showed a significant decrease of CBF in the right cerebellar hemisphere and cerebellar vermis. However, a significant reduction of CBF and CMRO2 was not observed in patients with Menzel type or Holmes type in these regions. In patients with LCCA and Holmes type, the severity of upper limb ataxia and dysdiadochokinesis were significantly correlated with CBF/mCBF and CMRO2/mCMRO2 in the cerebellar hemispheres and brainstem.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

[Comparison of anti-inflammatory, analgesic activities, anaphylactogenicity and acute toxicity between bee venom and its peptides].

Bee venom 1.0-2.0 mg/kg and bee venom peptides 1.0-2.0 mg/kg inhibited several inflammatory processes, such as ear swelling induced by xylene in mice, edema produced by injecting 1% carrageenin 0.1 ml beneath the plantar surface of hind paw in rats and showed a marked analgesic action induced by the hot plate and potassium antimony tartrate. Bee venom peptides had a markedly more effective action as compared with bee venom itself. The anaphylactogenicity of bee venom peptides was apparently milder than that of bee venom. The LD50 of bee venom ip in mice and bee venom peptides was 7.4 mg/kg and 7.9 mg/kg respectively.

Allergens↗
PubMed1992

On the mechanism by which bupivacaine conducts protons across the membranes of mitochondria and liposomes.

Bupivacaine and etidocaine possess the remarkable property of stimulating mitochondrial respiration to levels comparable with those observed with classical anionic protonophores (Dabadie, P., Bendriss, P., Erny, P., and Mazat, J.P. (1987) FEBS Lett. 226, 77-82). We show that these amphiphilic amines conduct protons across the membranes of mitochondria and liposomes and stimulate respiration by a true protonophoretic mechanism. The kinetics of drug-induced H+ flux exhibited integer Hill coefficients that were greater than two under all conditions, suggesting that multimers are required for H+ transport. When the energy barrier for ion transport was lowered in mitochondria, by increasing the membrane potential, or in liposomes, by adding phloretin, the Hill coefficients decreased to lower integer numbers. Protonophoretic activity depended exclusively on medium concentration of free base, leading us to conclude that bupivacaine and etidocaine conduct protons as associated, intramembrane multimers of the free base. Bupivacaine-induced H+ leak was ohmic rather than nonohmic, as would be expected of a mobile charged carrier. This kinetic behavior seems improbable for a multimeric mobile carrier mechanism and suggests a channel mechanism, in which ohmicity results from splitting of the energy barrier by energy wells along the transport pathway (Garlid, K. D., Beavis, A. D., and Ratkje, S. K. (1989) Biochim. Biophys. Acta 976, 109-120). We hypothesize that bupivacaine and etidocaine act by a novel "flickering channel" mechanism, in which transient linear complexes of free base molecules provide weak binding sites (energy wells) for protons within lipid bilayer membranes.

Animals↗
PubMed1992

Reconstitution, identification, purification, and immunological characterization of the 110-kDa Na+/Ca2+ antiporter from beef heart mitochondria.

The mitochondrial Na+/Ca2+ antiporter plays a key role in the physiological regulation of intramitochondrial Ca2+, which in turn attunes mitochondrial enzymes to the changing demands of the cell for ATP. We have now purified the Na+/Ca2+ antiporter from beef heart mitochondria by assaying detergent-solubilized chromatography fractions for reconstitutive activity. Na+ and Ca2+ transport were assayed using the fluorescent probes, sodium-binding benzofuran isophthalate and Fura-2, respectively. This approach enabled us to identify Na+/Ca2+ exchange activity with a 110-kDa inner membrane protein that catalyzed Na(+)-dependent Ca2+ transport and Ca(2+)-dependent Na+ transport. A new finding was that the Na+/Ca2+ antiporter also catalyzed Na+/Li+ exchange in the absence of Ca2+. All modes of transport were electroneutral and were inhibited by diltiazem and tetraphenylphosphonium cation. Monospecific polyclonal antibodies to the 110-kDa protein inhibited Na+/Ca2+ and Na+/Li+ exchange in the reconstituted system and recognized 110-kDa proteins in mitochondrial membranes isolated from rat heart, liver, and kidney.

Animals↗
PubMed1992

Identification of a novel receptor mediating substance P-induced behavior in the mouse.

To determine whether opioid receptors or the more recently characterized naloxone-sensitive substance P (SP) N-terminal binding sites play a role in desensitization to the behavioral effects of SP, we assessed the effects of selective antagonists at mu-(naloxonazine and beta-funaltrexamine), delta- (naltrindole) and kappa- (nor-binaltorphimine) opioid receptors, as well as the effect of [D-Pro2,D-Leu7]SP-(1-7) D-SP-(1-7) (D-SP (1-7)), an inhibitor of [3H]SP-(1-7) binding, on behaviors induced by intrathecally administered SP in mice. Whereas naloxone, a non-selective opioid antagonist, inhibited the development of behavioral desensitization to SP, the response to repeated SP administration remained unaffected by pretreatment with selective opioid antagonists. Like naloxone, however, the SP-(1-7) antagonist inhibited SP-induced desensitization. The protection against desensitization to SP by D-SP-(1-7), but not by selective antagonists of mu, delta or kappa receptors, suggests that desensitization to the behavioral effects of SP does not appear to be mediated by an action at an opioid receptor but by an action at the SP-(1-7) binding site.

Analysis of Variance↗