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Biomedical subjects

H Sun

Publications and source records attributed to H Sun.

At least 343 records · Page 19Linked to original sources
PubMed1997

Application of fuzzy graph theory to evaluation of human cardiac function.

To explore the possibility of application of the fuzzy graph theory to the evaluation of human cardiac function, the cardiac function of two groups of personnel working under special environment were evaluated using the method of fuzzy graph theory. The first group consists of 31 subjects aged 19-21 years. They were classified according to their cardiac function evaluated by the method of maximum support tree. While the second group consists of 24 subjects aged 30-40 years and were classified with fuzzy graph theory on the basis of 6 maximum principal components extracted from 16 physiological indices. Medical explanation of the results is convincing.

Adult↗
PubMed1997

[Changes of cardiac function during +Gz exposure in rabbits].

Changes of cardiac function was studied during +Gz exposure in rabbits. Seven New Zealand rabbits were anesthetized and exposed to +2, +4, and +6 Gz (each for 30s, onset rate 1G/s, with 15 min interval in between). The left ventricular systolic pressure (LVSP), peak rate of left ventricular pressure rising (+dp/dtmax) and ECG were recorded. The results showed that during +2, +4 and +6 Gz exposures, LVSP decreased by 62.96% (P<0.01), 63.34% (P<0.01) and 82.01% (P<0.01) respectively, and +dp/dtmax decreased by 58.46% (P<0.01), 53.59% (P<0.01) and 63.06% (P<0.01) respectively, and the left ventricular end diastolic pressure decreased by 67.78 % (P>0.05), 332.74 % (P<0.01) and 500.54% (P<0.01) respectively, as compared with those of control. It is suggested that cardiac function is depressed with +Gz exposure.

Acceleration↗
PubMed1997

[Serological survey of human T lymphotropic virus type I (HTLV-1) IgG antibody in south region of Xinjiang].

Human T lymphotropic virus type-1 (HTLV-1) is endemic in southwestern Japan, Seychelles Islands, Caribbean basin, Brazil, and Sub Saharan Africa. Recently, the prevalence of HTLV-1 of domestic source has been reported from Beijing, Fujian and so forth. The object of our study is to know whether the prevalence of HTLV-1 is present in Xinjiang. We collected 2642 serm samples of various ages and different nationalities (Uigur, Han and Khalkhas) from south region of Xinjiang and tested for determination of HTLV-1 IgG antibody by IFA. The results showed that the total positive rate of HTLV-1 IgG was 0.34% (9/2642), of which Uigur nationality was 0.74% (8/1082), Khalkhas nationality was 0.21 (1/471), Han nationality was zero (0/1089). This data indicated that there are HTLV-1 infection among the population of Xinjiang and especially in Uigur and Khalkhas. Why did the minority nationalities have relatively high frequency of HTLV-1 infection? This needs to be studied further.

Adolescent↗
PubMed1997

[Determination of molybdenum in natural waters by direct current plasma atomic emission spectrometry with ion-exchange preconcentration].

A new method was developed for the determination of trace molybdenum in natural waters by direct current plasma atomic emission spectrometry after separating and preconcentrating with D301 anion exchange resin. Mo adsorbed on the resin column can be recovered quantitatively by using 20mL of 8mol/L HNO3 at a flow rate of 0.6mL/min with elution rate of (81.6 +/- 1.78)%. The behaviour of Mo on the resin has been discussed. Simulative water and natural water samples have been determined. It was found that the interference element Ca could be separated effectively from Mo; an enrichment factor of 50 was obtained for Mo in 1L water sample; the determination limit of Mo was improved to 0.5 microg/L and the recovery of 90-107% was obtained.

Analytic Sample Preparation Methods↗
PubMed1997

Repair of incomplete simple syndactyly by a web flap on a subcutaneous tissue pedicle.

A new web flap on a subcutaneous tissue pedicle was developed to repair incomplete simple syndactyly. It was isolated from the top skin in syndactyly and transferred down into the depth of the web space to create a web commissure. With use of this technique, aesthetic appearance of the web and well-functioning fingers were gained. Moreover, this technique made full use of the original skin of the syndactyly, and a skin graft was not needed. We report here the operative technique, which presents another alternative for repair of incomplete simple syndactyly.

Adolescent↗
PubMed1997

Functional analysis of the nucleotide binding domains of the multidrug resistance protein (MRP).

HeLa cells were transfected with full-length multidrug resistance protein (MRP) cDNA and with MRP cDNAs that had been mutated at certain nucleotide binding domains. Stable transfectants were isolated and those producing equivalent amounts of P190 were tested in cytotoxicity assays using a variety of chemotherapeutic agents. The results demonstrate that deletions in the C-motif of NBD1 or the A-motif of NBD2 have a pronounced effect in reducing resistance levels to adriamycin, vincristine, or etoposide (VP-16). Single-site mutations of lysine in these same motifs reduce IC50 values but less than that observed with the deletion mutants. Additional studies have demonstrated an increase in drug accumulation and reduction in drug efflux in NBD deletion and single-site mutants. The results of this study therefore identify two lysines of the NBD A- and C-motifs that are critical for MRP-mediated multidrug resistance. The results also provide definitive evidence that resistance occurring as a result of MRP overexpression is related to enhanced levels of an ATP-dependent efflux pump.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1997

The role of cytoskeletal elements in the two-phase denucleation process of mammalian erythroblasts in vitro observed by laser confocal scanning microscope.

The cytoskeletal elements in the denucleation processes were observed using immunofluorescence and laser confocal scanning microscopy in the Friend virus (FVA) infected splenic erythroblasts of BALB/c mice. When cultured in the presence of erythropoietin (EPO), it was shown that the synchronized erythroid precursor cells proceeded to an autonomous nuclear extrusion when the three types of cytoskeletal elements were observed contributing to different phases of that process. The vimentin intermediate filament (IF) was shown as the nuclear anchorage elements with binding sites anchored from the nuclear lamina to the center as well as to the plasma membrane periphery. A dense perinuclear layer of vimentin fluorescence in erythroblasts was observable during the periods of 12, 24 and 36 hrs. in vitro culture. The amount of vimentin IF per cell was higher than that of tubulin and F-actin at 12-24 hrs. culture, but the vimentin filaments were observed to brake down and decreased steadily when the cells became differentiated into late erythroblasts at 36-48 hrs. Such an attenuation of vimentin filaments may facilitate the eccentric movement of the nucleus which can be regarded as the initial step (phase) of denucleation. The fluorescent intensity of tubulin and actin exhibited a significant rise and aggregated between the extruding nucleus and the incipient reticulocyte prior to and during the processes of denucleation, what indicated that the actin filaments and microtubules may play roles in the second phase of the denucleation process, or final commitment of enucleation. The erythroid differentiation-denucleation factor (EDDF), as an intrinsic factor, involved in the denucleation events, was also discussed.

Animals↗
PubMed1997

[Cloning and expression of promoter and signal peptide function fragments from Lactococcus lactis in Escherichia coli].

Promoter and signal peptide function fragments from Lactococcus lactis were cloned in E. coli using a promoter-signal sequence probe vector pGPB14. Forty-two clones were obtained, whose level of resistance to ampicillin ranged from 100 to 8000 micrograms/ml. Eight clones were selected for beta-lactamase distribution assay. The beta-lactamase activity was found mainly in the periplasm, which indicated successful secretion of the enzyme. Southern hybridization test demonstrated that the inserted fragments were indeed from L. lactis. Restriction enzyme analysis revealed that the size of inserted fragments ranged from 80bp to 400 bp, four of which were sequenced on the vector pGEM-3Zf. It was found that the inserted fragments of pSEQ8 and pSEQ12 turned out to be part of the inserted fragments of pSEQ4 and pSEQ17 respectively. Promoter and translation initiation codon were found among all four fragments signal sequenced. One typical S. D. sequence and one atypical signal sequence were found in pHSB4 and pHSB8, while the other two contained no typical S. D. sequence and signal peptide sequence. In addition, it was found that the upstream regions of the promoter contributed to the efficiency of transcription initiation.

Base Sequence↗
PubMed1997

[Protective effect of interleukin-1 beta on acetaminophen induced liver damage in mice].

In the model of liver damage induced by acetaminophen of mice, injection of interleukin-1 beta (IL-1 beta, i.p. 50,000 U/kg) 1, 6 or 12 h before the administration of acetaminophen could reduce the leakages of GPT and GOT induced by acetaminophen, with the 12 h pretreatment being the most effective. Treatment with IL-1 beta 1 h after administration of acetaminophen had no effect. Treatment with IL-1 beta of different doses (10,000, 30,000 or 50,000 U/kg) 12 h before the administration of acetaminophen could reduce the leakages of transaminases in a dose dependent manner and decrease the mortality of mice. The protective effect of IL-1 beta on the liver could be abolished by IL-1 beta receptor antagonist. Further experiments showed that IL-1 beta could increase the content of reduced glutathione (GSH) in normal liver and reverse the decline of GSH and the increase of GSSG induced by acetaminophen. IL-1 beta could also reduce malondiadehyde (MDA) content enhanced by acetaminophen. The above results indicate that the preventive effect of IL-1 beta against liver damage due to acetaminophen may be mediated through IL-1 beta receptor by increasing glutathione synthesis and decreasing lipid peroxidation of the liver.

Acetaminophen↗
PubMed1997

[Involvement of nitric oxide and cGMP in the protective effect of neurotensin on hepatocytes].

In the present work, the relation of cytoprotection of neurotensin to nitric oxide (NO), cGMP and cAMP was investigated in primary cultured mouse hepatocytes. The results are as follows: After administration of acetaminophen (20 mmol/L) to the medium, the leakage of GOT and GPT increased significantly. Pretreatment with neurotensin (10(-7) mol/L) before acetaminophen reduced the leakage of GOT and GPT. No synthase inhibitor, L-NAME, completely blocked the cytoprotective effect of neurotensin. Neurotensin could enhance the intracellular cGMP content, but had no effect on cAMP content. These results indicate that the protective effect of neurotensin on hepatocytes is mediated by NO probably by enhancing intracellular cGMP content.

Acetaminophen↗
PubMed1997

[The spontaneous otitis media in rickety rats].

This paper is aimed to study the incidence and hearing impairment of spontaneous otitis media in rickety rats during a longterm vitamin D deficient breeding. Thirty Sprague-Dawley rats ranged from 20 to 25-day-old were used, and vitamin D deficient rickets models were established. Another thirty rats were used as the normal control. It was found that both normal and rickety rats had the possibilities of suffering from otitis media (mainly exudative) during the two-month-breeding. The incidence of otitis media in normal rats was 5% (3 from 60 ears), while that in the rickety ones was 16.67% (10 from 60 ears). It is believed that a rickety sufferer may be in higher danger of having otitis media than the normal one.

Action Potentials↗
PubMed1996

Rationalization of the strength of metal binding to human serum transferrin.

A wide range of metal ions of natural, therapeutic, diagnostic and toxic interest are transported by serum transferrin (80 kDa). It is therefore important to understand the factors that control the strength of metal binding. We show here that even though Sc3+ has only slightly larger ionic radius than Fe3+ (0.075 nm versus 0.065 nm), it binds to the C-lobe and N-lobe sites much more weakly: logK1* (bicarbonate-independent binding constant) 14.6 +/- 0.2, logK2* 13.3 +/- 0.3, respectively (10 mM Hepes, 5 mM bicarbonate, 310 K). Preferential binding to the C-lobe was established by 1H-NMR spectroscopy. We show that the strength of binding of divalent and trivalent metal ions to human serum transferrin correlates with metal ion acidity [and therefore with the strength of binding to hydroxide, K1(OH)]. The correlations are of predictive value for a range of other metal ions. The plot of logK1* (human serum transferrin) versus logK1(OH) has a negative intercept consistent with unfavorable entropy effects due to lobe closure of apotransferrin on binding of metal ions. This interpretation was tested by comparison with similar correlations of the strength of metal binding to the enzymes carbonic anhydrase and carboxypeptidase with that for the low-M(r) ligand imidazole. These plots have positive intercepts consistent with the preorganized (entatic) state of these metalloenzymes (favorable entropy effects on metal binding).

Binding Sites↗
PubMed1996

Two distinct mechanisms for long-range patterning by Decapentaplegic in the Drosophila wing.

Secreted signalling molecules provide cells with positional information that organizes long-range pattern during the development of multicellular animals. Evidence is presented that localized expression of Decapentaplegic instructs cells about their position along the anterior-posterior axis of the Drosophila wing in two distinct ways. One mechanism is based on the local concentration of the secreted protein; the other is based on the ability of the cells to retain an instruction received at an earlier time when their progenitors were in close proximity to the signal. Both mechanisms are involved in axis formation.

Animals↗
PubMed1996

Unexpectedly strong binding of a large metal ion (Bi3+) to human serum transferrin.

Large metal ions (>0.9 A ionic radius) have previously been found to bind only weakly to human serum transferrin (hTF, 80 kDa), presumably because the interdomain cleft cannot close around the metal and synergistic anion. Surprisingly, therefore, we report that Bi3+ (ionic radius 1.03 A), a metal ion widely used in anti-ulcer drugs, binds strongly to both the N- and C-lobes with log K1* = 19.42 and log K2* = 18.58 (10 mM Hepes, 5 mM bicarbonate, 310 K). The uptake of Bi3+ by apo-hTF from bismuth citrate complexes is very slow (hours), whereas that from bismuth nitrilotriacetate is rapid (minutes). Evidence from absorption and NMR spectroscopy is presented to show that Bi3+ binds to the specific Fe3+ binding sites along with carbonate as the synergistic anion. Under the conditions used, preferential binding of Bi3+ to the C-lobe of hTF is observed. Linear free energy relationships show that there is a strong correlation between the strength of binding of Bi3+ and Fe3+ to a wide variety of ligands which include transferrin. Therefore we conclude that the strength of metal ion binding to transferrin is determined more by the ligand donor set than by the size of the ion.

Bismuth↗
PubMed1996

Activation of Gsalpha by the epidermal growth factor receptor involves phosphorylation.

Previous studies from our laboratory have shown that epidermal growth factor (EGF) stimulates cAMP accumulation in the heart via a process involving Gsalpha and the EGF receptor (EGFR) protein tyrosine kinase activity (Nair, B. G., Parikh, B., Milligan, G., and Patel, T. B. (1990) J. Biol. Chem. 265, 21317-21322; Nair, B. G., and Patel, T. B. (1993) Biochem. Pharmacol. 46, 1239-1245). Therefore, studies were performed to investigate the hypothesis that the EGFR protein tyrosine kinase phosphorylates Gsalpha and activates this protein. Employing purified EGFR and Gsalpha, we have demonstrated that the EGFR kinase phosphorylates Gsalpha in a time-dependent manner with a stoichiometry of 2 mol of phosphate incorporated/mol of Gsalpha. As determined by phosphoamino acid analysis, the phosphorylation of Gsalpha by the EGFR kinase was exclusively on tyrosine residues. Interestingly, GDP and guanosine 5'-3-O-(thio)triphosphate (GTPgammaS) inhibited the phosphorylation of Gsalpha without altering EGFR autophosphorylation. However, G protein betagamma subunits protected against GDP- and GTPgammaS-mediated inhibition of phosphorylation of Gsalpha. In functional studies, phospho-Gsalpha demonstrated a greater GTPase activity and also a greater capacity to bind GTPgammaS as compared to the nonphosphorylated Gsalpha. Moreover, the phospho-Gsalpha augmented adenylyl cyclase activity in S49 cyc- cell membranes to a greater extent than its nonphosphorylated counterpart. Therefore, we conclude that phosphorylation of Gsalpha on tyrosine residues by the EGFR kinase activates this G protein and increases its ability to stimulate adenylyl cyclase.

Adenylyl Cyclases↗
PubMed1996

Surgical denervation increases protein tyrosine phosphatase activity in skeletal muscle.

Protein tyrosine phosphorylation, which plays an important role in synapse formation at the neuromuscular junction, appears to be regulated by presynaptic neurons. Innervation increases whereas denervation decreases the phosphotyrosine content at the neuromuscular junction. The innervation-dependent tyrosine phosphorylation may result from elevated activity of protein tyrosine kinases; alternatively innervation may down-regulate the protein tyrosine phosphatase activity in the skeletal muscle. To investigate the possible neuronal control of protein tyrosine phosphatase activity at the neuromuscular junction, we have characterized protein tyrosine phosphatase activity in rat skeletal muscle and studied the effects of surgical denervation on the phosphatase activity. Protein tyrosine phosphatase activity in the skeletal muscle, assayed using src [32P]-phosphorylated myelin basic protein as a substrate, was both time- and protein concentration-dependent and was inhibited by micromolar concentrations of vanadate and zinc ion, both of which are known to inhibit tyrosine phosphatases specifically. It was not affected, however, by chemicals known to inhibit acid and alkaline phosphatases or serine/threonine phosphatases. Surgical denervation caused an increase in protein tyrosine phosphatase activity in rat hindlimb muscles. The increase in phosphatase activity reached a maximum (2-fold above the normal) 4 days post-denervation and maintained a plateau for up to 24 days. The biochemical properties of the phosphatase activity in denervated muscle were similar to those of the phosphatase activity in the innervated muscles. These results demonstrate that protein tyrosine phosphatase activity in skeletal muscle is regulated by motoneurons.

Animals↗
PubMed1996

Regulation of peroxisome proliferator-activated receptor-alpha mRNA in rat liver.

Chemical-induced peroxisome proliferation in rodent liver is postulated to occur via activation of members of the steroid hormone receptor superfamily, the peroxisome proliferation-activated receptors (PPARs). In the present study, the expression of the predominant liver subtype PPAR alpha was examined and compared to that of acyl-CoA oxidase (ACO), a marker for peroxisome proliferation and a prototype for genes regulated via PPARs. Despite the induction of both mRNA species in vivo by the peroxisome proliferator perfluorodecanoic acid (PFDA), dose response and time course indicate PPAR alpha and ACO are not controlled similarly. Messenger RNA levels for ACO increased rapidly in rat liver and declined over the subsequent 7 days following PFDA administration, while PPAR alpha mRNA increased slower and remained elevated over this period. In addition, PPAR alpha mRNA accumulation in PFDA-treated rats appears to be due primarily to hypophagia as pair feeding and complete caloric restriction result in a large increase in the concentration of this messenger RNA. Nuclear run-on experiments in vivo suggest that, unlike ACO, PFDA as well as caloric restriction results in accumulation of PPAR alpha mRNA which cannot be explained solely by transcriptional activation. These data indicated that PPAR alpha mRNA accumulation has a very small peroxisome proliferator-dependent component and that other factors may be involved. A rat hepatoma cell line was examined to determine the direct effect on peroxisome proliferators on PPAR alpha mRNA. PPAR alpha and ACO mRNA levels were increased rapidly in the rat hepatoma cell line FaO after treatment with PFDA or the prototypical peroxisome proliferator Wy 14,643. In this cell line, PPAR alpha mRNA levels are not affected by glucagon or insulin and in addition to peroxisome proliferators are induced in this cell line by oleic acid and dexamethasone. The latter treatment had the greatest effect on PPAR alpha mRNA accumulation while having a minimal effect on ACO mRNA. Treatment of FaO cells with actinomycin D prior to Wy 14,643 abolished ACO and PPAR alpha mRNA accumulation, demonstrating that there must be a transcriptional component of the peroxisome proliferator response. Therefore, although PPAR alpha is responsive to peroxisome proliferators and direct effects are observed in cell cultures, mRNA accumulation in vivo is predominantly posttranscriptional, and endogenous regulators such as glucocorticoids may play critical roles in the tissue- and developmentally specific expression of this steroid hormone receptor.

Acyl-CoA Oxidase↗