Search PubMed⌕ Search

Biomedical subjects

H Xue

Publications and source records attributed to H Xue.

At least 109 records · Page 6Linked to original sources

Inactivation of lipid-enveloped and non-lipid-enveloped model viruses in normal human plasma by crosslinked starch-iodine.

BACKGROUND: The purpose of this study was to evaluate an iodine-based method of activating potentially harmful viruses that might be found in normal human plasma. STUDY DESIGN AND METHODS: A procedure has been developed for inactivating lipid-enveloped and non-lipid-enveloped model viruses in normal human plasma by using iodine complexed to crosslinked potato starch. The established conditions are an iodine concentration of 1.05 mg per mL and 60 minutes' incubation. RESULTS: Under these conditions, inactivation of more than 9 log10 of vesicular stomatitis virus, a lipid-enveloped virus, and more than 7 log10 of encephalomyocarditis virus, a non-lipid-enveloped virus, was achieved, with minimal losses of biologic activity of selected plasma proteins. Under these conditions, 70 percent of factor VIII activity, 77 percent of factor IX activity, and 100 percent of protein C activity in the plasma were retained. CONCLUSION: Crosslinked starch-iodine may be useful in the inactivation of viruses in single-donor plasma units and in pooled human plasma before fractionation.

Blood↗

Vascular mechanisms of cyclosporin-induced hypertension in the rat.

Numerous studies have explored the pathogenesis of cyclosporin A (CysA)-induced hypertension; however, none has assessed the impact of CysA treatment on resistance arteries in the setting of elevated blood pressure. Therefore, we studied the chronic effect of CysA on rat mesenteric artery resistance vessels (ex vivo). CysA (25 mg/kg per d for 7 d), but not vehicle, significantly raised systolic blood pressure (13.4 +/- 2.2 mmHg, P < 0.003, n = 9 per group). The resistance vessels from CysA-treated rats showed a small but significant decrease in norepinephrine sensitivity (P < 0.03) and a pronounced decrease in endothelium-dependent and -independent relaxation (P < 0.001) compared to controls. Endothelin-1 sensitivity tended to be diminished (P = 0.07). The direct (in vitro) effect of CysA was subsequently evaluated in resistance vessels from nontreated animals (n = 8) and exposed to CysA (2 micrograms/ml) for 24 h. As observed in vivo, CysA significantly decreased endothelium-dependent and -independent relaxations (P < 0.05) and attenuated norepinephrine sensitivity (P = 0.06). Methylene blue, a nitric oxide quencher, significantly inhibited the acetylcholine-induced relaxation in control, but not in CysA vessels, suggesting a selective action of CysA on the nitric oxide pathway. We conclude that CysA-induced hypertension is the consequence of a primary effect on resistance vessel relaxation, not increased vasoconstriction, as previously suggested.

Acetylcholine↗

[Relationship between the sex of Schistosoma japonicum and circulating antigen detection].

Single sex cercariae were used to infect rabbits and the detection of circulating membrane antigen by dot-ELISA were followed up until 1 year postinfection. 9 rabbits infected with male cercariae (worm recovery 15-133, mean 53.1) and 9 rabbits infected with female cercariae (worm recovery 1-102, mean 39.1) were examined but no positive reaction was occurred. On the contrary, 7 rabbits infected with bi-sex cercariae (worm recovery 4-161, mean 67.1) all showed positive reactions 6-10 wks post-infection. Uni-sex female worms usually could not develop to maturity within rabbits even 1 year after infection, suggesting that the life-span of uni-sex female worm might be 1 year at least in rabbits. The uni-sex male worms could develop to maturity, being usually stout. The question why no circulating membrane antigen (even CCA, unpublished data) could be detected and the nature of antigen we detected needs further investigation.

Animals↗

1,25(OH)2 vitamin D3-induced alterations in vascular reactivity in the spontaneously hypertensive rat.

Recent studies showed that 1,25(OH)2 vitamin D3 stimulates calcium uptake in vascular smooth muscle cells resulting in increased vascular reactivity. Despite reliable effects on vascular tissue, daily injections of 1,25(OH)2 vitamin D3 have not consistently altered basal blood pressure. In the current study, 1,25(OH)2 vitamin D3 was examined for vascular reactivity in vitro as well as blood pressure reactivity in vivo. 1,25(OH)2 vitamin D3 was either injected as a daily subcutaneous dose of 48 ng/kg or placed in an osmotic minipump that was implanted subcutaneously and delivered at a rate of 2/ng/kg/hr (48 ng/kg/d). Blood pressure reactivity to bolus injections of norepinephrine (NE) and angiotensin II (AII) was tested after 1, 6, and 7 days of 1,25(OH)2 vitamin D3 treatment. On the seventh day, the animals were killed and rings from the aorta and mesenteric artery were placed in a muscle bath for measurement of vascular reactivity to NE and potassium chloride. Vessels from animals injected with 1,25(OH)2 vitamin D3 had significantly greater responses to NE (p < 0.001) and potassium chloride (p < 0.001) than those from minipump or control animals. There was no significant difference in baseline BP across treatment conditions or any reliable difference in blood pressure reactivity to NE or AII. The data showed that 1,25(OH)2 vitamin D3 can enhance vascular reactivity without altering baseline blood pressure or blood pressure reactivity. Moreover, intermittent administration of calcitriol may enhance vascular reactivity to norepinephrine and potassium chloride to a greater extent than the same dose of calcitriol given as a continuous infusion.

Animals↗

Intracellular Ca2+ and force generation determined in resistance arteries of normotensive and hypertensive rats.

OBJECTIVE: Dysfunctional cellular Ca2+ handling has been proposed to underlie the heightened vascular reactivity observed in the spontaneously hypertensive rat (SHR) model of genetic hypertension. We tested the hypothesis that basal or agonist-induced mobilization of intracellular Ca2+ is elevated in mesenteric resistance arteries of SHR compared with the normotensive Wistar-Kyoto (WKY) rat. DESIGN: A method using fura-2 for the simultaneous measurement of intracellular Ca2+ and isometric force generation in isolated mesenteric resistance arteries was employed to measure agonist-induced changes in Ca2+ and force during activation with 100 mmol/l K+ or 10 mumol/l norepinephrine. Arteries with normalized diameter 220-240 microns from male rats aged 14-15 weeks were examined. RESULTS: No differences were detected between the rat strains in basal Ca2+ concentration or the steady-state concentration of Ca2+ achieved in response to either 100 mmol/l K+ or 10 mumol/l norepinephrine. The relationship between Ca2+ and force during the contractile responses to K+ and norepinephrine was analyzed. No differences between the strains in the level of active stress, normalized to unit intracellular Ca2+, were detected in the steady-state responses to K+ or norepinephrine. CONCLUSIONS: The present results do not support the hypothesis that alterations in either the basal concentration of intracellular Ca2+ or the amount of intracellular Ca2+ mobilized in response to high levels of norepinephrine or K+ are present in resistance arteries of SHR compared with those of WKY rats. Moreover, these findings suggest that elevations in Ca2+ do not contribute to heightened peripheral resistance in SHR.

Animals↗

Mevalonate availability and cardiovascular functions.

Data delineating the relationship between disorders of cholesterol metabolism and elevated blood pressure (BP) do not exist. We postulated that mevalonate, the metabolic precursor of endogenous cholesterol and the direct product of 3-hydroxy-3-methylglutaryl-CoA reductase, was a contributing factor for the maintenance of vascular tone and systemic BP. We conducted in vivo, ex vivo, and in vitro experiments in normotensive and hypertensive rats, where exogenous mevalonate and lovastatin, a competitive inhibitor of 3-hydroxy-3-methylglutaryl-CoA reductase, were used, respectively, to increase or limit mevalonate availability. Mevalonate decreased BP in the whole animal without significant change in plasma cholesterol. Incubation of aortas with mevalonate attenuated their reactivity to norepinephrine and increased their response to endothelium-dependent and -independent relaxing factors. Lovastatin, in contrast, had the opposite effect in vivo and in vitro: it increased BP, enhanced vascular response to norepinephrine, and impaired endothelium-dependent and -independent relaxations. Neither agent modified cholesterol vascular content. Alteration of vascular reactivity was also observed in resistance vessels from animals pretreated with lovastatin. Our findings suggest that mevalonate availability is an unrecognized metabolic contributor to vascular tone and BP. They imply that (i) metabolites of the mevalonate pathway other than cholesterol could potentially control vascular functions and cardiovascular hemodynamics, (ii) elevated arterial pressure could be in part the consequence of primary disorders of this pathway, and (iii) pharmacological inhibition of mevalonate production as a means to lower plasma cholesterol may have an adverse impact on other cardiovascular risk factors, such as BP.

Acetylcholine↗

Modified nucleotides in Bacillus subtilis tRNA(Trp) hyperexpressed in Escherichia coli.

In the present study, modified nucleotides in the B. subtilis tRNA(Trp) cloned and hyperexpressed in E. coli have been identified by TLC and HPLC analyses. The modification patterns of the two isoacceptors of cloned B. subtilis tRNA(Trp) have been compared with those of native tRNA(Trp) from B. subtilis and from E. coli. The modifications of the A73 mutant of B. subtilis tRNA(Trp), which is inactive toward its cognate TrpRS, were also investigated. The results indicate the formation of the modified nucleotides S4U8, Gm18, D20, Cm32, i6A/ms2i6A37, T54 and psi 55 on cloned B. subtilis tRNA(Trp). This modification pattern resembles the pattern of E. coli tRNA(Trp), except that m7G is missing from the cloned tRNA(Trp), probably on account of its short extra loop. In contrast, the pattern departs substantially from that of native B. subtilis tRNA(Trp). Therefore, the cloned B. subtilis tRNA(Trp) has taken on largely the modification pattern of E. coli tRNA(Trp) despite the 26% sequence difference between the two species of tRNA, gaining in particular the Cm32 and Gm18 modifications from the E. coli host. A notable difference between the isoacceptors of the cloned tRNA(Trp) was seen in the extent of modification of A37, which occurred as either the hypomodified i6A or the hypermodified ms2i6A form. Surprisingly, base substitution of guanosine by adenosine at position 73 of the cloned tRNA(Trp) has led to the abolition of the 2'-O-methylation modification of the remote G18 residue.

Bacillus subtilis↗

Identity elements of tRNA(Trp). Identification and evolutionary conservation.

In this study, the varying reactivities of Bacillus subtilis tryptophanyl-tRNA synthetase toward prokaryotic, eukaryotic, and halophile tRNAs were employed to define the potential identity elements on tRNA(Trp). On this basis mutagenesis was performed to obtain, through in vivo heterologous expression in Escherichia coli and in vitro transcription with T7 RNA polymerase, mutant B. subtilis tRNA(Trp) for comparison with the wild-type. These comparisons served to establish G73 and the anticodon as major identity elements, and A1-U72, G5-C68, and A9 as minor identity elements. While the tryptophanyl-tRNA synthetase from B. subtilis and E. coli require G73 to function, replacement of G73 by A73 favors the enzyme from yeast. This change points to the variation of the identity elements for the same amino acid among different organisms. The similarity in these elements between B. subtilis and E. coli tryptophanyl-tRNA synthetase, however, suggests that identity elements on tRNA, like the active centers on enzymes, undergo evolutionary change at slower rates than less essential portions of the macromolecule.

Animals↗

Crystallization of Bacillus subtilis tryptophanyl-tRNA synthetase.

Tryptophanyl-tRNA synthetase from Bacillus subtilis was overexpressed in Escherichia coli and was purified using column chromatography on DEAE-Sephacel and hydroxyapatite columns. Single crystals of the synthetase were grown by vapor diffusion at 4 degrees C from pH 5.5 solutions of polyethylene glycol 8000 containing magnesium ATP and L-tryptophan. The crystals diffracted to about 4.0 A resolution at -150 degrees C and appeared to belong to the orthorhombic space group P2(1)2(1)2 with unit cell dimensions: a = 143.6 A, b = 111.6 A, c = 50.6 A with one dimer in the asymmetric unit.

Bacillus subtilis↗

Purification of hyperexpressed Bacillus subtilis tRNA(Trp) cloned in Escherichia coli.

To study the effects of evolutionary sequence changes on the molecular interactions of tRNA inside the cell, the Bacillus subtilis tRNA(Trp) gene has been cloned into Escherichia coli JM109 under the control of the lac promotor. Hyperexpression of the gene in minimal medium upon induction yielded 28% of total tRNA in the form of B. subtilis tRNA(Trp). The tRNA(Trp) gene product was purified by the use of a single Vydac C4 high-performance liquid chromatography (HPLC) matrix. This experimental system provided a valuable system for the hyperexpression and purification of a heterologous tRNA for studies in vitro. Moreover, because HPLC fractionation of the heterologous tRNA(Trp) gene product yielded multiple peaks, the system made possible an analysis of the molecular mechanisms for the transcriptional modifications of the tRNA(Trp) gene product in vivo.

Bacillus subtilis↗

Forty-year experience with second malignancies after treatment of childhood cancer: analysis of outcome following the development of the second malignancy.

As the cure rate for childhood malignancies increases, the number of patients at risk for development of second malignancies also increases. Due to the potentially long remaining life span, long-term follow-up is difficult and patients are often at risk after presumptive cures. Some authors believe that cure rates for second malignancies are similar to cure rates for primary malignancies. We reviewed the records of 162 patients seen at our institution who had developed a second malignancy after treatment for childhood cancer. Presentation, age at diagnosis, tumor histology, extent of tumor, treatment (including radiotherapy with dosage when available, and chemotherapy) plus outcome were recorded. Mean age at diagnosis of the primary malignancy was 10.3 years. The most common primary malignancy was Hodgkin's disease (33) followed by soft tissue sarcoma (28), retinoblastoma (20), bone tumor (17), central nervous system (CNS) tumor (13), leukemia (8), Wilms' tumor (7), non-Hodgkin's lymphoma (6), neuroblastoma (5), thyroid neoplasm (5), and others (20). The average interval between diagnosis of the first and second malignancy was 10.8 years. These second tumors carried a high mortality. Only 56 patients have no evidence of disease. Five patients are known to be alive with disease and 92 patients have expired due to their second malignancy. Disease status in 8 patients is unknown. The most common second malignancy was osteosarcoma (35) followed by soft tissue sarcoma (24), breast cancer (15), leukemia (14), thyroid carcinoma (14), CNS tumors (12), melanoma (8), nonmelanomatous skin cancer (8), lymphoma (5), and others (27).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

On the vascular inotropic action of 1,25-(OH)2 vitamin D3.

Previous work from our laboratory showed that injection of 1,25-(OH)2 vitamin D3 (1,25-vitD) into the rat over a 3-day period increases force generating capacity of subsequently isolated resistance arteries. To better understand the mechanism of this vascular inotropic action, we examined the time course of its development and Ca(2+)-associated mechanism of action. Mesenteric resistance arteries were isolated from 12-week-old male spontaneously hypertensive rats (SHR) 6 and 24 h after a single injection and 24 h after three and seven consecutive days of injection of 1,25-vitD (20 ng/100 g) or vehicle. Serum 1,25-vitD was increased nearly threefold at 6 h, but not at later times. Serum total and ionized Ca2+ were not affected at any time point. No changes in contractile force generation were detected at 6 and 24 h, but a significant increase in the active stress response to norepinephrine and arginine vasopressin was observed after both 3 and 7 days of 1,25-vitD treatment. No effect on sensitivity to either agonist was observed at any time point. To determine whether the vascular inotropic effects of 1,25-vitD might translate into changes in blood pressure, 11-week-old male Wistar rats were given daily injections of 1,25-vitD (20 ng/100 g) over a 4-week period, and blood pressure and body weight were measured. While body weight did not differ at any time point in the two groups, systolic blood pressure was elevated in the 1,25-vitD group v control by 7 days, and continued to be elevated over the period of observation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Effect of chronic and subacute parathyroidectomy on blood pressure and resistance artery contractility in the spontaneously hypertensive rat.

OBJECTIVE: Chronic parathyroidectomy (PTX) attenuates blood pressure and increases vascular force generation. The mechanism is not understood. We tested the hypothesis that PTX-induced changes in blood pressure and vessel contractility result from rapid changes in serum parameters induced by PTX, and the hypothesis that the endothelium-derived factors contribute to PTX-induced enhancement of force generation in the spontaneously hypertensive rat (SHR). DESIGN: Chronic PTX or sham surgery was performed on 5-week-old male SHR, and subacute PTX was performed on 13- to 14-week-old SHR. The following experimental parameters were measured 5-6 weeks after chronic and 2 days after subacute PTX: systolic blood pressure, serum Ca2+, 1,25-dihydroxyvitamin D3 (vitD) and mesenteric resistance artery contractility. RESULTS: Chronic PTX significantly reduced blood pressure, body weight and serum Ca2+ compared with sham surgery; subacute PTX reduced only serum Ca2+ and vitD. Compared with sham surgery, the mesenteric resistance artery following chronic PTX showed increased active stress responses to norepinephrine and serotonin that were not associated with changes in free intracellular Ca2+, but were abolished by endothelial denudation. Subacute PTX did not affect the active stress response to norepinephrine or endothelin. Low-dose acetylcholine induced relaxation that was attenuated in the chronic, but not the subacute, PTX subgroup compared with the sham-operated subgroup. High-dose acetylcholine induced contraction that was significantly greater in the chronic, but not subacute, PTX rats than in sham-operated rats. Indomethacin abolished the acetylcholine-induced contraction in all groups, but did not improve the impaired relaxation response of the chronic PTX subgroup. CONCLUSIONS: The PTX-induced decrease in blood pressure and increase in force generation do not result from acute changes initiated by reduction of serum parathyroid hormone, vitD or Ca2+. Moreover, the PTX-induced increase in force generation results from a decrease in the production of a non-cyclo-oxygenase endothelium-dependent relaxing factor.

Animals↗

Streptozotocin and alloxan are comparable agents in the diabetic model of impaired wound healing.

This study compares the drugs Streptozotocin (STZ) and Alloxan (ALN) in the diabetic wound healing model to determine the effect of their diverse immunologic and metabolic activity upon wound collagen and collagenase. Levels of hydroxyproline (as a measure of collagen) and collagenase were determined in polytetrafluorethylene (PTFE) wound cylinders harvested from STZ and ALN-diabetic rats and nondiabetic controls on post-operative days 5, 10 and 20. Animals treated with STZ and ALN had significantly less hydroxyproline on day 5 compared to control rats (p < 0.05). However, no difference was noted on days 10 and 20 between these two agents and controls, or between STZ and ALN at any time in the experiment. Despite their markedly dissimilar side effects, we conclude that either drug is appropriate in the diabetic wound healing when determining wound collagen and collagenase activity in this setting.

Alloxan↗

[An immunoelectron microscopic study of growth hormone secretory granules in human pituitary].

Two fetal and 8 adult pituitaries as well as 12 pituitary growth hormone (GH) cell adenomas were studied with immunoelectron microscopy using immunogold double labelling. The secretory granules in the GH cells were GH-immunoreactive, and there were no differences in size, electron density and morphology among the samples. Large, pleomorphic secretory granules were often seen in the GH cell adenomas: they were GH-immunoreactive and prolactin-negative. The authors except that double labelling with immunogold will be useful for clarifying the nature of the large, pleomorphic secretory granules.

Acromegaly↗

Overexpression and amplification of c-myc and c-Ha-ras oncogenes in pleomorphic salivary adenoma.

Twenty-seven samples of pleomorphic salivary adenoma (PSA) were examined for expression and structure of c-myc, c-Ha-ras, c-erbB-2, c-sis oncogenes by RNA dot blot, DNA dot blot and Southern blot hybridization. Eighteen of 25 PSA showed 5.02 +/- 4.74 fold overexpression of c-myc oncogene, 6 of 19 PSA had 4.91 +/- 3.87 fold overexpression of c-Ha-ras oncogene. Two of 16 PSA were found to have overexpression of c-erbB-2 oncogene. In addition, 7 of 10 PSA and 1 of 9 PSA were detected to have c-myc and c-erbB-2 oncogene amplification respectively. However, no rearrangement, amplification or overexpression of c-sis gene was found. We also discussed various clinicopathological parameters of PSA, which however, had no significant correlation with expression of c-myc or c-Ha-ras oncogene. Our results indicate that activation of c-myc, c-Ha-ras and their combination may play an important role in the pathogenesis of PSA.

Adenoma, Pleomorphic↗

Antiproliferative and endothelium-dependent vasodilator properties of 1,3-dihydro-3-p-chlorophenyl-7-hydroxy-6-methyl-furo-(3,4c) pyridine hydrochloride (cicletanine).

The vasodilator and antiproliferative actions of 1,3-dihydro-3-p-chlorophenyl-7-hydroxy-6-methyl-furo-(3,4c) pyridine hydrochloride (cicletanine) were studied on mesenteric resistance arteries and cultured mesenteric artery myocytes of spontaneously hypertensive (SHR) and normotensive Wistar Kyoto (WKY) rats. Cicletanine (20-200 microM) induced relaxation of endothelium-intact mesenteric resistance arteries of SHR and WKY precontracted with norepinephrine. No difference in sensitivity was observed (SHR IC50 = 77 +/- 12 microM vs. 83.3 +/- 7.4 microM for WKY, N.S.). Endothelial denudation of WKY vessels significantly attenuated the relaxing action of cicletanine (IC50 + endo = 83 +/- 7.4 microM vs. IC50 - endo = 135 +/- 9.7 microM; P < .001) and had a similar, but nonsignificant effect on SHR (IC50 + endo = 77 +/- 12 microM vs. IC50 - endo = 117 +/- 14.5 microM; P = .065). Preincubation of endothelium-intact vessels with nitro-L-arginine methyl ester significantly attenuated cicletanine-induced relaxation in WKY, but not SHR vessels; 0.1 mM Ba++ had a similar effect. Preincubation with 3 microM indomethacin was without effect on relaxation of vessels of either strain. Cicletanine (100-1000 microM) inhibited proliferation of cultured superior mesenteric artery muscle cells growing in the presence of either 10% (SHR IC50 = 440 +/- 24 microM vs. 517 +/- 12 microM for WKY; P < .05) or 2% fetal bovine serum. This antiproliferative action was fully reversible, partially inhibited by indomethacin in SHR myocytes and was associated with a decrease in [3H]thymidine uptake in both strains.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗