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Biomedical subjects

X Sun

Publications and source records attributed to X Sun.

At least 343 records · Page 19Linked to original sources
PubMed1998

[The enzymes activity of intestine grafts after combined small bowel/liver transplantation in rats].

OBJECTIVE: To study the alteration of the enzymes activity of intestine grafts after combined small bowel/liver transplantation in rats and the relations between their changes, functions and immune rejection. METHOD: A kind of model of combined small bowel/liver transplantation (SLT) was established in SD closed colony rats. The enzymes activity of grafts were examined at regular postoperative intervals with histochemical methods. RESULT: The enzymes activity of grafts disappeared eventually in isolated small bowel transplantation rats. Contrary, those in SLT rats were remained and recovered after operation. CONCLUSION: The rejection in grafted intestine can be prevented or delayed in SLT rats. The examination of activity of enzymes and nerves in grafts may be used to monitor rejection and study function of grafts.

Animals↗
PubMed1998

[Simultaneous determination of aspartame and amino acids in fermented milk beverages by HPLC].

An RP-HPLC method for the simultaneous determination of aspartame and amino acids in fermented milk beverages were established. Samples were prepared by mixing with methanol at a ratio of 1:1 and centrifuged at 4,000 r/min for 15 min. Ten microL supernatant was moved into a sample tube, dried and derivatized according to PICO-TAG procedure developed by Waters. A Novapak C18 column (3.9 mm x 150 mm) was used instead of PICO TAG column and the gradient elution program was modified correspondingly. Column temperature was maintained at 38 degrees C and the components were detected at 254 nm. Linearity for aspartame at the range in 1-100 mg/L is A = 333 C + 20 with r = 0.9996 where A is the integrated area of chromatographic peak of aspartame and C is the corresponding mass concentration. Repeatability for 8 injections was tested and the RSD of 3.2% was obtained. The recovery of aspartame for 5 samples with the method ranged from 94.2% to 98.7%.

Amino Acids↗
PubMed1998

[Method for determination research of trace germanium in the serum of cancer patients by graphite furnace atomic absorption spectrometry].

Using a tungstate-coated graphite tube, trace germanium in serum samples was determined by Zeeman graphite AAS with NH4NO3 as a matrix modifier. The sensitivity of Ge can be significantly improved. The matrix interference has been removed. The relative standard deviation is less than 3.61%. The method is simple, rapid and accurate.

Blood Chemical Analysis↗
PubMed1998

[Determination of trace Al in serum of cancer patients by graphite furnace atomic absorption spectrometry using K2Cr2O7 and surfactant as matrix modifier with molybdenate coated tubes].

Different kinds of graphite tubes and of matrix modifiers have been tested for optimization of operation condition for determination of Al in serum by GFAAS. The effects of different interference ions have been eliminated by adding K2Cr2O7 and Triton X-100 as matrix modifier. The method is suitable for determination of serum of cancer patients. The characteristic mass is 21.15pg/0.0044 A x S. The recovery rate is 104.92. The relative standard deviation is less than 8.17%. The result obtained is satisfactory.

Aluminum↗
PubMed1998

[Indirect determination of pyritic sulfur in coal by flame atomic absorption spectrometry].

An atomic absorption spectrophotometric method for the determination of pyritic sulfur in coal was developed based on oxidizing pyritic sulfur in coal into sulfate, which then reacted on an excess of solid barium chromate,and was followed by collection of the unreacted barium chromate and barium sulfate precipitates, and AAS determination of free chromate (equivalent to the sulfur originally present) at 357.9nm. The method was applied satisfactorily to the determination of pyritic sulfur in coal samples. The recovery of sulfur was 95 -102% and relative standard deviation 3-5%.

English Abstract↗
PubMed1998

[Study of determination method for trace cobalt in serum of cancer patients].

A method for the determination of micro amount of Co in serum of cancer patients by GFAAS has been established. The effect of protein in serum was eliminated by adding (1+1) HNO3. The blood serum was determined directly by adding Triton X-100 and NH4VO3 as matrix modifier. The method is handy and fast. The rate of recovery is 97.60-102.21% with RSD < 7.21.

Blood Chemical Analysis↗
PubMed1998

Antibody to caspase-cleaved actin detects apoptosis in differentiated neuroblastoma and plaque-associated neurons and microglia in Alzheimer's disease.

During apoptosis, activation of a family of cysteine proteases related to interleukin-1beta-converting enzyme (ICE)-related proteases or "caspases" results in endoproteolytic cleavage of multiple substrates at specific aspartate residues. We have sought to develop new antibody probes for the neoepitopes in protein fragments produced by ICE-related proteolytic cleavage as specific markers of events tightly linked to apoptotic mechanisms. Here, we demonstrate that an antibody probe specific for the C terminus of a 32-kd actin fragment produced by ICE-like activity specifically labels apoptotic but not necrotic, differentiated human neuroblastoma cells in culture. Unlike probes for nonspecific DNA strand breaks confined to the nucleus or cell body, this method allows the detection of cytoskeletal fragments in cell processes as well as the perikaryon long before DNA fragmentation and cell death and therefore serves as a novel marker of apoptosis-related events in distal parts of cells such as axons and dendrites. To illustrate this new tool, we show that the antibody detects the processes and cell bodies of degenerating neurons and plaque-associated microglia in Alzheimer's disease. In situ detection of caspase-cleaved actin provides a new means to evaluate the role of caspase activation in pathological and physiological processes.

Actins↗
PubMed1998

Real time analysis of lung sounds.

This paper describes a real time system for the analysis of pulmonary sounds. The system performs various types of time-domain and spectrographic analysis. It is able to display time-domain waveforms obtained from microphones detecting lung sounds, their power spectra and a real-time linear prediction model instantaneously for the immediate identification of interesting features. Details of the system are presented with examples of clinical research carried out using spectrographic analysis.

Bias↗
PubMed1997

Molecular structure of a functional Drosophila centromere.

Centromeres play a critical role in chromosome inheritance but are among the most difficult genomic components to analyze in multicellular eukaryotes. Here, we present a highly detailed molecular structure of a functional centromere in a multicellular organism. The centromere of the Drosophila minichromosome Dp1187 is contained within a 420 kb region of centric heterochromatin. We have used a new approach to characterize the detailed structure of this centromere and found that it is primarily composed of satellites and single, complete transposable elements. In the rest of the Drosophila genome, these satellites and transposable elements are neither unique to the centromeres nor present at all centromeres. We discuss the impact of these results on our understanding of heterochromatin structure and on the determinants of centromere identity and function.

Animals↗
PubMed1997

Developmental changes in regulation of the Na+, K(+)-ATPase alpha 3 isoform by thyroid hormone in ferret heart.

Ferret heart expresses the alpha 1- as well as the alpha 3-isoform of the Na+, K(+)-ATPase. We have shown previously that the alpha 3 isoform is differentially upregulated during postnatal cardiac development and that in adult ferrets expression of alpha 3 is not responsive to regulation by thyroid hormone (TH). Since developmental-stage dependent effects of TH have been reported previously, the present study examined whether effects of TH on expression of the Na+, K(+)-ATPase isoforms in ferret heart is modulated during development and possible mechanisms were examined. Ferrets of different age groups were treated with TH and the relative abundance of Na+, K(+)-ATPase isoforms in ferret myocardium was determined by immunoblotting. Thyroid hormone (T3; 50 micrograms/100 g body weight on 3 alternating days, s.c.) increased protein levels of the alpha 3 isoform, but not that of alpha 1 or beta 1, in myocardium of 5-day-old and 3-week-old ferrets. By contrast, in myocardium of 6- and 8-week-old ferrets T3 failed to increase protein levels of alpha 1 and alpha 3. To determine whether elevated plasma levels of TH during development plays a role in the transition, mature ferrets were first made hypothyroid before TH treatment. In these hypothyroid ferrets expression of the alpha 3 isoform remained unresponsive to TH (T4, 0.5 mg/kg for 7 days, s.c.). The transition from TH-responsive to TH-unresponsive appears to be isoform-specific because in skeletal muscle of 8-week-old ferrets and in hypothyroid ferrets the alpha 2 isoform is upregulated by TH. Finally, there appears to be functional thyroid hormone receptors throughout development because in each age group TH effectively induced expression of alpha-MHC in the myocardium. In conclusion, these findings demonstrate that expression of alpha 3 isoform in the myocardium of newborn ferret is responsive to TH; however, the responsiveness terminates between 3- and 6-weeks of age. Neither elevated endogenous TH level nor a lack of functional thyroid hormone receptor appears to be responsible for the transition from TH-responsive to TH-unresponsive.

Animals↗
PubMed1997

Increased production of extracellular glutamate by the mitochondrial glutaminase following neuronal death.

Elevated extracellular concentrations of the excitatory transmitter glutamate are an important cause of neuronal death in a variety of disorders of the nervous system. The concentrations and rates of clearance and production of extracellular glutamate were measured in the medium of primary cultures from mouse neocortex containing neurons, astrocytes, or both cell types. Measurements were performed in the presence and absence of 2 mM glutamine with or without neuronal injury caused by 5-h exposure to hypoxia or 500 microM N-methyl-D-aspartate or a freeze-thaw cycle. High rates of glutamate generation (0.5-0.8 microM/min in the 0.4-ml culture well) occurred if neurons were both damaged and exposed to glutamine. Intact neurons or glia exposed to glutamine generated only small amounts of glutamate (0.03 microM/min). Glutamate generation by damaged neurons was dependent on the presence of glutamine, activated by phosphate, and inhibited by 6-diazo-5-oxo-L-norleucine and p-chloromercuriphenylsulfonic acid (pCMPS), strongly implicating the mitochondrial glutaminase. Following 5-h exposure to 500 microM N-methyl-D-aspartate, the glutaminase was localized to fragments of damaged neurons and was accessible to inhibition by the membrane-impermeant pCMPS. The glutaminase activity from damaged neurons is sufficient to account for the neurotoxic concentrations of glutamate in hypoxic mixed neuronal-glial cultures exposed to 2 mM glutamine. Finally, pCMPS is neuroprotective and also prevents the increased rate of generation of glutamate observed in neuronal cultures after prolonged exposure to glutamine. The cumulative data indicate the following: 1) excitotoxic neuronal death activates the hydrolysis of extracellular glutamine by the mitochondrial glutaminase, and 2) the glutaminase in damaged neurons is sufficient to cause neuronal death in in vitro models of neuronal injury.

4-Chloromercuribenzenesulfonate↗
PubMed1997

Reduction of vesicular acetylcholine transporter mRNA in the rat septum following lead exposure.

We have previously observed that maternal exposure to lead (Pb) results in a reduction of levels of mRNA coding for cholineacetyltransferase (ChAT) in the septum of developing rat without affecting the dams. Here we report that Pb similarly affects the expression of vesicular acetylcholine transporter (VAChT) mRNA in the rat septum. In close agreement with the time course of ChAT mRNA expression, septal VAChT mRNA levels increased from 30% at postnatal day 7 to 78% and 100% of adult levels at days 14 and 21, respectively. Maternal exposure to 0.2% lead acetate in drinking water from gestational day 16 resulted in an approximately 30% reduction of VAChT in 7 and 21-day-old rat pups without affecting VAChT mRNA levels in the dams. These results indicate a developmental stage-dependent interference by Pb with ChAT/VAChT gene expression in the rat septum.

Acetylcholine↗
PubMed1997

Hypoxia, but not reoxygenation, induces interleukin 6 gene expression through NF-kappa B activation.

Interleukin (IL) 6 is one of major mediators of inflammation, and IL-6 gene activation during hypoxia/reoxygenation has been implicated in the pathogenesis of ischemia/reperfusion injury. However, molecular events involved in IL-6 gene expression during hypoxia/reoxygenation remain to be identified. We have previously shown that NF-kappa B plays an essential and indispensable role in the transcriptional activation of the IL-6 gene induced by various stimuli, including IL-1 and tumor necrosis factor-alpha. We show here that hypoxia, but not reoxygenation, induces the activation of NF-kappa B through the degradation of a major inhibitor of NF-kappa B, I kappa B alpha. This hypoxia-induced NF-kappa B activation resulted in the kappa B-dependent transcriptional activation of the IL-6 gene. Interestingly, the time course of hypoxia-induced NF-kappa B activation was rather slow as compared with those of NF-kappa B activation induced by other stimuli, such as IL-1: a significant NF-kappa B activation was not observed before 1 hr of hypoxia treatment and persisted for up to 7 hr of hypoxia treatment. However, hypoxia-induced NF-kappa B activation was not inhibited by cycloheximide, which indicates that hypoxia directly triggers NF-kappa B activation. Furthermore, while hypoxia is unlikely to generate reactive oxygen intermediates, pretreatment of cells with antioxidants such as N-acetyl cysteine and alpha-tocopherol inhibited NF-kappa B activation induced by hypoxia. Thus, we discuss possible implications of these results for a postulated role of reactive oxygen intermediates in NF-kappa B activation.

Animals↗
PubMed1997

Depression of the inotropic action of isoprenaline by nitric oxide synthase induction in rat isolated hearts.

The mechanisms involved in myocardial dysfunction during septic shock are not well understood. We have investigated the effects of endotoxin and the role of nitric oxide (NO) in the beta-adrenoceptor responsiveness of rat isolated, ejecting hearts perfused at 60 mmHg of head pressure. In vivo pretreatment with endotoxin (4 mg/kg, i.p., 3 h before heart isolation) significantly attenuated the inotropic response (increase in left ventricular developed pressure, LVP) to isoprenaline (0.15 microgram) after 30 min equilibration and after a further 90 min of perfusion. The peak rate of LVP development (dP/dtmax) in response to isoprenaline was reduced by endotoxin pretreatment, as was the increase of coronary flow. The depression of ventricular contraction was prevented by pretreatment with dexamethasone (1 mg/kg, i.p., 30 min before endotoxin), and was also restored by perfusion with NG-nitro-L-arginine (L-NA, 10 microM) for 60 min, but not by NG-nitro-D-arginine (D-NA, 10 microM). Mercaptoethylguanidine (MEG, 30 microM), a selective inhibitor of the inducible NO synthase (isoform 2), also reversed the depression of the isoprenaline response caused by endotoxin pretreatment. However, treatment with endotoxin, dexamethasone, L-NA, D-NA or MEG had minimal effects on the baseline parameters of LVP, dP/dtmax and coronary flow, which all tended to decline over the 2 h perfusion period. Western blot analysis using an antibody to NO synthase (isoform 2, but not to isoform 3) revealed the induction of a protein corresponding to NO synthase 2 in the endotoxin-treated hearts but not in control hearts or those treated with dexamethasone or MEG. In summary, these results indicate the endotoxin depresses myocardial contractile function and reduces inotropic responsiveness to beta-adrenoceptor activation. The effect of endotoxin on the inotropic response is mediated, at least in part, by products of an endogenous NO synthase that is suppressed by dexamethasone and a specific inhibitor of NO synthase (isoform 2).

Adrenergic beta-Agonists↗
PubMed1997

Calmodulin in ischemic neurotoxicity of rat hippocampus in vitro.

To determine whether calmodulin plays a role in neurodegeneration after ischemia, effects of the selective calmodulin inhibitors calmidazolium and W7 were studied in organotypic cultures of rat hippocampus. Protection of pyramidal cells in the CA1 region of the hippocampus by calmidazolium and W7 against hypoxia/hypoglycemia suggests that activation of intracellular calmodulin plays a significant role in ischemic neuronal injury. Both ryanodine and TMB-8, inhibitors of intracellular Ca2+ release, failed to prevent ischemic neuronal injury. These results indicate that calmodulin, a major intracellular Ca2+ binding protein, plays a significant role in experimental ischemia-induced hippocampal neuronal injury in vitro.

Animals↗
PubMed1997

Nonenzymatic anticoagulant activity of the mutant serine protease Ser360Ala-activated protein C mediated by factor Va.

The human plasma serine protease, activated protein C (APC), primarily exerts its anticoagulant function by proteolytic inactivation of the blood coagulation cofactors Va and VIIIa. A recombinant active site Ser 360 to Ala mutation of protein C was prepared, and the mutant protein was expressed in human 293 kidney cells and purified. The activation peptide of the mutant protein C zymogen was cleaved by a snake venom activator, Protac C, but the "activated" S360A APC did not have amidolytic activity. However, it did exhibit significant anticoagulant activity both in clotting assays and in a purified protein assay system that measured prothrombinase activity. The S360A APC was compared to plasma-derived and wild-type recombinant APC. The anticoagulant activity of the mutant, but not native APC, was resistant to diisopropyl fluorophosphate, whereas all APCs were inhibited by monoclonal antibodies against APC. In contrast to native APC, S360A APC was not inactivated by serine protease inhibitors in plasma and did not bind to the highly reactive mutant protease inhibitor M358R alpha 1 antitrypsin. Since plasma serpins provide the major mechanism for inactivating APC in vivo, this suggests that S360A APC would have a long half-life in vivo, with potential therapeutic advantages. S360A APC rapidly inhibited factor Va in a nonenzymatic manner since it apparently did not proteolyze factor Va. These data suggest that native APC may exhibit rapid nonenzymatic anticoagulant activity followed by enzymatic irreversible proteolysis of factor Va. The results of clotting assays and prothrombinase assays showed that S360A APC could not inhibit the variant Gln 506-FVa compared with normal Arg 506-FVa, suggesting that the active site of S360A APC binds to FVa at or near Arg 506.

Alanine↗
PubMed1997

Identification and characterization of growth hormone receptors in snakehead fish (Ophiocephalus argus cantor) liver.

The specific binding of 125I-labeled fish growth hormone (GH) to hepatic membranes prepared from several freshwater fish was assessed. A high level of growth hormone receptor (GHR) was detected on the hepatic membranes of the snakehead fish (Ophiocephalus argus Cantor). Scatchard analysis of the binding data showed a single class of high affinity binding site with a binding affinity (Ka) of 1.45 +/- 0.23 x 10(9) M-1 and a binding capacity (Bmax) of 198 +/- 57 fmol/mg protein. The binding was specific for fish GH and was saturable. In addition, the specific binding was temperature- and time-dependent, reaching a steady state after 16 hr of incubation at 25 degrees . The molecular weight of GHR as measured by Sephadex G-200 column chromatography and Western blot analysis using a monoclonal antibody (Mab263) against GHR was found to be 200-400 and 90-93 kDa, respectively. Two bands at 65 and 89 kDa were identified in ligand crosslinking studies of membrane receptors. A sensitive teleost GH radioreceptor assay (RRA) was developed, using recombinant fish GH and a membrane preparation from snakehead fish liver, capable of measuring bioactive GH in fish sera or other samples.

Animals↗