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Biomedical subjects

D Xue

Publications and source records attributed to D Xue.

At least 37 records · Page 2Linked to original sources
PubMed1998

Glioma prostaglandin levels correlate with brain edema.

The present study was designed to prospectively investigated the prostaglandin (PG) levels and extent of peritumoral edema in 30 cases of glioma by using methods of radioimmunoassay and imaging. Both TXB2 and 6-keto-PGF1 alpha levels in all glioma groups went up over that in the control group. TXB2 level and ratio of TXB2/6-keto-PGF1 alpha were markedly increased with the extent of tumor malignancy. Water concentration in anaplastic astrocytoma and glioblastoma were significantly elevated. Difference in TXB2 level and TXB2/6-keto-PGF1 alpha ratio among three edema grades were statistically significant. TXB2 level and ratio of TXB2/6-keto-PGF1 alpha were closely correlated with water concentration (r1 = 0.53, r2 = 0.72, P < 0.01). Our findings suggested that the metabolism of PG in glioma were in the state of disorder, and that the imbalance between PGI2 and TXA2 may be one of factors which affect the formation of peritumoral edema.

6-Ketoprostaglandin F1 alpha↗
PubMed1998

Hormone secretion by cell culture of human GH-PRL secreting pituitary adenomas: effects of bromocriptine.

Dopamine agonists effectively reduce the secretion of prolactin (PRL) in the great majority of prolactinomas and reduce the bulk of the adenomas, as well as have partial therapeutic effect on some patients with acromegaly. The inhibitory effect of bromocriptine (BC), a dopamine agonist, on growth hormone (GH) and PRL secretion of dispersed cells from the pituitary adenomas of 16 cases of acromegaly, which secret GH and PRL simultaneously, were evaluated in vitro. The significant inhibitory effects of BC on PRL secretion were found in 12 cases. It was also found that PRL secretion was strongly inhibited when GH was suppressed; on the contrary, when GH secretion was not suppressed, the production of PRL was not or weakly inhibited. The exact mechanism of the effects is unclear so far. It is necessary to investigate, at molecular level, the etiology of GH-PRL adenomas and its response to therapeutic agents.

Adenoma↗
PubMed1998

The bidirectional effect of vanadyl ion on the oxygen affinity of human hemoglobin.

The bidirectional effects of vanadyl on the oxygen affinity of hemoglobin depend on the mole ratio of vanadyl to Hb(R). In low R, the vanadyl ion increases Hb's oxygen affinity due to DPG hydrolysis. The lowered oxygen affinity in higher R is mainly due to the reactive-oxygen-species, probably superoxide, induced oxidation of Fe(II)-Hb to Fe(III)-Hb. The conformation change due to vanadyl binding contribute also to the lowered oxygen binding, but is monotonously decreasing with increasing of R values.

Circular Dichroism↗
PubMed1997

Phosphorylation of IkappaB-alpha inhibits its cleavage by caspase CPP32 in vitro.

IkappaB proteins function as direct regulators of Rel/NF-kappaB transcription complexes. We show that the cell-death protease CPP32 (caspase-3) in vitro specifically cleaved chicken and human IkappaB-alpha at a conserved Asp-Ser sequence. This cleavage site appears to be identical to the site at which chicken IkappaB-alpha is cleaved in vivo in temperature-sensitive v-Rel-transformed chicken spleen cells undergoing apoptosis. Other caspases, namely interleukin-1beta-converting enzyme (caspase-1) and Ich-1 (caspase-2), did not cleave IkappaB-alpha. CPP32 also cleaved mammalian IkappaB-beta in vitro at the analogous Asp-Ser sequence. Cleavage of IkappaB-alpha by CPP32 was blocked by serine phosphorylation of IkappaB-alpha. Cleavage of IkappaB-alpha by a CPP32- like protease could generate a constitutive inhibitor of Rel transcription complexes. This report provides evidence for a direct biochemical interaction between the NF-kappaB signaling pathway and a cell-death protease signaling pathway.

Animals↗
PubMed1997

Caenorhabditis elegans CED-9 protein is a bifunctional cell-death inhibitor.

The Caenorhabditis elegans gene ced-9 prevents cells from undergoing programmed cell death and encodes a protein similar to the mammalian cell-death inhibitor Bcl-2. We show here that the CED-9 protein is a substrate for the C. elegans cell-death protease CED-3, which is a member of a family of cysteine proteases first defined by CED-3 and human interleukin-1beta converting enzyme (ICE). CED-9 can be cleaved by CED-3 at two sites near its amino terminus, and the presence of at least one of these sites is important for complete protection by CED-9 against cell death. Cleavage of CED-9 by CED-3 generates a carboxy-terminal product that resembles Bcl-2 in sequence and in function. Bcl-2 and the baculovirus protein p35, which inhibits cell death in different species through a mechanism that depends on the presence of its cleavage site for the CED-3/ICE family of proteases, inhibit cell death additively in C. elegans. Our results indicate that CED-9 prevents programmed cell death in C. elegans through two distinct mechanisms: first, CED-9 may, by analogy with p35, directly inhibit the CED-3 protease by an interaction involving the CED-3 cleavage sites in CED-9; second, CED-9 may directly or indirectly inhibit CED-3 by means of a protective mechanism similar to that used by mammalian Bcl-2.

Animals↗
PubMed1997

Effect of temperature in focal ischemia of rat brain studied by 31P and 1H spectroscopic imaging.

31P, 1H and lactate spectroscopic imaging was used to evaluate' the effects of hypothermia on focal cerebral ischemia produced by middle cerebral artery occlusion. The effects on high energy phosphate metabolism, pH, lactate and NAA were investigated in 24 spontaneously hypertensive rats subjected to either permanent or transient ischemia. Under either normothermic (37.5 degrees C) or hypothermic (32 degrees C) conditions, with permanent 6-h occlusion, there was little difference between groups in either the NMR measurements or the volume of infarction. In animals that underwent 3 h of ischemia followed by 12 h of reperfusion, the ischemic changes in lactate, pH, NAA, and high-energy phosphate returned toward control values, and there was a protective effect of hypothermia (infarct volume of 211 +/- 26 and 40 +/- 14 mm3 in normothermic and hypothermic groups, respectively). Thus, hypothermia did not ameliorate the changes in lactate, pH, NAA, or high energy phosphate levels occurring during ischemia, however, during reperfusion there was an improvement in both the recovery of these metabolites and pathological outcome in hypothermic compared with normothermic animals.

Adenosine Triphosphate↗
PubMed1997

Relationship between invasiveness of pituitary somatotrophinomas and structural abnormalities of protein kinase C gene in human.

The potential role of the protein kinase C (PKC) transduction system in controlling proliferation of human pituitary somatotrophinomas was investigated. Twenty somatotrophinomas were studied using PCR and direct sequencing methods. No point mutation within the alpha PKC gene, previously thought to be associated with invasive pituitary tumors, was found in any of the 20 somatotrophinomas. It is concluded that PKC transduction system may play an important role in controlling pituitary somatotrophinoma proliferation, but there is no correlation between invasiveness and the previously reported alpha PKC gene mutation.

Adenoma↗
PubMed1997

[Chemical constituents of Cistanche tubulosa (Schenk) Wight].

From the dry bulbs of Cistanche tubulosa six compounds were isolated and identified as beta-sitosterol, D-mannitol, daucosterol, succinic acid, D-glucose and D-fructose by spectral and chemical analyses. All of them were isolated from the plant for the first time.

Cycadopsida↗
PubMed1997

The La protein in Schizosaccharomyces pombe: a conserved yet dispensable phosphoprotein that functions in tRNA maturation.

Most RNA polymerase III transcripts are bound immediately after synthesis by an abundant nuclear phosphoprotein known as the La autoantigen. Experiments performed in the budding yeast Saccharomyces cerevisiae have revealed that binding of the La protein to tRNA precursors is required for the endonucleolytic maturation of the 3' terminus of many tRNAs. In the absence of this protein, the 3' ends of these tRNAs are trimmed by exonucleases (Yoo CJ, Wolin SL, 1997, Cell 89:393-402). Here we report the characterization of the La protein in the fission yeast Schizosaccharomyces pombe. As was described for budding yeast, S. pombe cells lacking the La protein are viable and exhibit alterations in the pathway of pre-tRNA maturation. Introduction of either the human, S. cerevisiae, or S. pombe La protein into these cells restores the detected pattern of tRNA processing intermediates to that of wild-type cells. By performing immunoprecipitations from cells that were metabolically labeled with 32P-orthophosphate, we demonstrate that the S. pombe and S. cerevisiae La proteins, like the human La protein, are phosphorylated in vivo. Thus, although the La protein is dispensable for growth in these yeasts, both the structure of the protein and its function in pre-tRNA maturation have been highly conserved throughout evolution.

Amino Acid Sequence↗
PubMed1996

The Caenorhabditis elegans cell-death protein CED-3 is a cysteine protease with substrate specificities similar to those of the human CPP32 protease.

The Caenorhabditis elegans cell-death gene ced-3 encodes a protein similar to mammalian interleukin-1beta-converting enzyme (ICE), a cysteine protease implicated in mammalian apoptosis. We show that the full-length CED-3 protein undergoes proteolytic activation to generate a CED-3 cysteine protease and that CED-3 protease activity is required for killing cells by programmed cell death in C. elegans. We developed an easy and general method for the purification of CED-3/ICE-like proteases and used this method to facilitate a comparison of the substrate specificities of four different purified cysteine proteases. We found that in its substrate preferences CED-3 was more similar to the mammalian CPP32 protease than to mammalian ICE or NEDD2/ICH-1 protease. Our results suggest that different mammalian CED-3/ICE-like proteases may have distinct roles in mammalian apoptosis and that CPP32 is a candidate for being a mammalian functional equivalent of CED-3.

Amino Acid Sequence↗
PubMed1995

Inhibition of the Caenorhabditis elegans cell-death protease CED-3 by a CED-3 cleavage site in baculovirus p35 protein.

The baculovirus protein p35 inhibits programmed cell death in such diverse animals as insects, nematodes and mammals. Here we show that p35 protein is a substrate for and inhibitor of the Caenorhabditis elegans cell-death protease CED-3 (refs 6, 7) and a substrate for four CED-3-like vertebrate cysteine protease activities implicated in apoptosis in mammals. A p35 mutation that greatly reduced p35 activity in vitro as a CED-3 substrate and inhibitor abolished p35 activity in vivo in protecting against cell death in C. elegans. Introduction of the CED-3 cleavage site in p35 into the cowpox virus protein crmA, which inhibits mammalian apoptosis but not programmed cell death in C. elegans, caused crmA to block CED-3-mediated cell death. These observations suggest that p35 may prevent programmed cell death in C. elegans and other species by acting as a competitive inhibitor of cysteine proteases.

Amino Acid Sequence↗
PubMed1995

Stable expression of rat cytochrome P450 11 beta-hydroxylase (CYP11B1) and aldosterone synthase (CYP11B2) in MA-10 cells.

Glucocorticoids and mineralocorticoids are synthesized in the adrenal cortex through the action of two different cytochrome 11 beta-hydroxylases, CYP11B1 (11 beta-hydroxylase) and CYP11B2 (aldosterone synthase) which are distributed in the zona fasciculata and glomerulosa, respectively. We have created stably transfected cell lines using the Leydig tumor cell line MA-10 with CYP11B1 and CYP11B2 cDNA-containing plasmids which have a selectable gene to confer resistance to geneticin. The expression of the transfected cDNA in the cells was characterized by Northern-blot and measurement of enzymatic activity. The cell lines express the enzymes stably for many generations. CYP11B1 transfected cells converted DOC into corticosterone, 18-OH-DOC and small amounts of 18-OH-corticosterone, in a time and concentration dependent manner. Incubation of the cells with corticosterone generated 18-OH-corticosterone especially at concentrations of 30 and 100 microM. The production of 18-OH-corticosterone from corticosterone at these doses was significantly higher than incubations with similar concentrations of DOC. CYP11B2 transfected cells converted DOC into corticosterone, 18-OH-corticosterone, aldosterone and small amounts of 18-OH-DOC in a time and concentration dependent manner. They converted corticosterone into 18-OH-corticosterone and aldosterone in a time and concentration dependent manner. The absolute and relative production of aldosterone from DOC was significantly higher than when cells were incubated with corticosterone, and the ratio of aldosterone to 18-OH-corticosterone was higher at all concentrations of DOC compared to corticosterone. CYP11B2 transfected cells (but not the CYP11B1 transfected cells) transform 18-OH-DOC into 18-OH-corticosterone, but can not convert 18-OH-DOC into aldosterone. In conclusion, stably transfected MA-10 cells with the cDNAs for the CYP11B1 and CYP11B2 enzymes were prepared and their enzymatic activity studied. These cells are useful in the study of inhibitors of the specific enzymes, as well as determining the roles that each enzyme plays in zone-specific steroidogenesis in the adrenal cortex.

18-Hydroxycorticosterone↗
PubMed1995

[Active antisenile constituents in Cistanche deserticola Y. C. Ma].

From the dry bulbs of Cistanche deserticola a branch of orobahchacease plant growing in Inner Mongolia two active antisenile constituents (D-mannitol and polysaccharide) were isolated and identified. Chemical analysis and spectroscopic tests show that D-mannitol corresponds to the authentic standard, and polysaccharide is condensed from rhamnose, xylose, arabinose and galactose.

Aging↗
PubMed1994

The hybrid rat cytochrome P450 containing the first 5 exons of the CYP11B1 and last 4 exons from the CYP11B2 enzyme retains 11 beta-hydroxylase activity, but the alternative hybrid is inactive.

Human, mouse and rats have 2 different cytochrome P-450 11 beta-hydroxylases in the adrenal cortex. The classical rat 11 beta-hydroxylase or CYP11B1 enzyme hydroxylates deoxycorticosterone to corticosterone and 18-hydroxydeoxycorticosterone and is located throughout the adrenal. The second aldosterone synthase or CYP11B2 enzyme is located in the zona glomerulosa and converts deoxycorticosterone to corticosterone, 18-hydroxycorticosterone and aldosterone. In rat the coding nucleotide sequence and the deduced amino acid sequences of the CYP11B1 and CYP11B2 genes are homologous by 88% and 83%, respectively. We have constructed two different hybrid cDNAs by exchanging two fragments of the rat CYP11B1 and CYP11B2 at the junction of the 5/6 exon and expressed them in COS 7 cells. The hybrid CYPH11B1 construct containing the first 5 exons of the CYP11B1 when expressed, retains 11 beta-hydroxylase activity, but cannot process corticosterone to 18-hydroxycorticosterone or aldosterone. The hybrid CYPH11B2 construct containing the first 5 exons of the CYP11B2 enzyme when expressed is inactive.

Animals↗
PubMed1994

DNA damage consistent with apoptosis in transient focal ischaemic neocortex.

Transient focal ischaemia was produced in rat right neocortex by temporary middle cerebral artery occlusion. DNA damage was visualized in situ in cells of this right hemisphere but not in the contralateral hemisphere. The extracted damaged DNA exhibited laddered fragmentation which is indicative of apoptotic degradation. The amount of DNA damage was quantified by an end-labelling technique and shown to increase with the duration of the ischaemic insult. We conclude that the neurodegeneration resulting from focal ischaemia has an apoptotic component.

Animals↗
PubMed1994

Failure to prevent selective CA1 neuronal death and reduce cortical infarction following cerebral ischemia with inhibition of nitric oxide synthase.

We investigated the putative role of nitric oxide in the expression of neuronal injury following both transient severe forebrain ischemia (CA1 neuronal injury) and transient or permanent middle cerebral artery occlusion (neocortical pannecrosis). Using the four-vessel occlusion model and increasing doses of N-omega-nitro-L-arginine, 2-40 mg/kg, we were unable to demonstrate any reduction in the percentage of CA1 cells injured following 10 min of transient severe forebrain ischemia followed by seven days of reperfusion. Higher doses proved toxic insofar as they increased the mortality following the ischemic insult. Saline-treated animals (n = 8) had 77 +/- 10% CA1 injury while those treated with 2 mg/kg of nitro-arginine i.v. had 80 +/- 7% (n = 7), and those with 10 mg/kg i.v. had 78 +/- 11% (n = 8). Two of five rats given 20 mg/kg i.v., three of eight given 40 mg/kg i.v., and two of six given 10 mg/kg i.v. followed by 3 x 10 mg/kg i.p., died. Of those treated with high-dose nitro-arginine and which survived ischemia and seven days' reperfusion, no significant reduction in CA1 injury was detected. Wistar rats and spontaneously hypertensive rats treated with either saline or nitro-arginine i.v. were exposed to 2 h of transient middle cerebral artery occlusion followed by 22 h of reperfusion. There were seven animals in each group. Wistars treated with saline had 198 +/- 67 mm3 (mean +/- S.D.) of neocortical infarction, and those treated with 10 m/kg of nitro-arginine i.v. had 199 +/- 93 mm3. Spontaneously hypertensive rats, transiently ischemic, treated with saline had 164 +/- 25 mm3 of infarct volume, while those treated with 2 mg/kg i.v. had 151 +/- 53 mm3, and those treated with 10 mg/kg i.v. had 145 +/- 29 mm3. Animals treated with 40 mg/kg i.v. had a nonsignificantly larger mean infarct volume (191 +/- 81 mm3). High dose nitro-arginine caused an increase in hypertension in the spontaneously hypertensive rats and increased the severity of focal ischemia as measured by intra-ischemic regional cerebral blood flows. A final group of seven spontaneously hypertensive rats underwent permanent middle cerebral artery occlusion and repeated dosing with N-omega-nitro-L-arginine i.p. In these animals an infarct volume of 234 +/- 60 mm3 was observed, which was again not statistically different from saline-treated controls (208 +/- 43 mm3, n = 7).(ABSTRACT TRUNCATED AT 400 WORDS)

Amino Acid Oxidoreductases↗