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Biomedical subjects

Q Xu

Publications and source records attributed to Q Xu.

At least 289 records · Page 16Linked to original sources
PubMed1997

Lethal and Sublethal Effects of Nitrogen Fertilizer Ammonium Nitrate onCommon Toad (Bufo bufo) Tadpoles

The impact of elevated ammonium nitrate concentrations onthe survival and development of common toad (Bufo bufo) tadpoles wasinvestigated in the laboratory. 1,704 mg/L and 1,637 mg/L nitrate (equivalentto 2,198.7 mg/L and 2,112.3 mg/L ammonium nitrate) were recorded as 96 h and168 h LC50s respectively. These are well above field levels (10-250 mg/L)observed in freshwater in Britain. The exposure of tadpoles to nominalconcentration of 100 mg/L nitrate for 24, 48, and 72 h caused a significantdecrease in their activity but no clear reduction in food consumption ordelay of the development. In subchronic exposures at the nominalconcentrations of 50 and 100 mg/L nitrate, the metamorphosis started earlierand took less time to complete than in the control. However, some of theresults were equivocal, at 50 mg NO3/L the metamorphs weresignificantly larger than the controls, while at 100 mg NO3/Lmetamorphs were not significantly different from the controls. Certaindeformities and unusual swimming patterns were also found in tadpoles exposedto various concentrations of ammonium nitrate.

Journal Article↗
PubMed1997

One-shot delayed-type hypersensitivity reaction in the mouse liver causes a sustained liver injury to picryl chloride.

The developmental characteristics of liver injury induced by a delayed-type hypersensitivity (DTH) mechanism against picryl chloride were examined for 9 consecutive weeks in 3 mouse strains, BALB/c, Kunming and ICR mice. The changes of most biochemical parameters were similar in these three strains, namely, the activities of serum transaminases, lactic dehydrogenase, and prolidase were elevated significantly on day 1, during the first several weeks, and almost throughout the duration, respectively, of liver injury. The content of liver hydroxyproline was also increased after 1-9 weeks of liver injury. In addition, a significant decrease of liver weight, serum alkaline phosphatase and albumin level was observed in BALB/c and Kunming mice. Similar changes in liver histology were also found in the three strains. The hepatocellular necrosis and inflammatory infiltration into the portal area were the predominant features on day 1 and were still distinct during the subsequent several weeks. The mild or moderate hepatocellular degeneration, regeneration and connective tissue hyperplasia were observed after 1 or 3 weeks. A bridging necrosis between portal and portal was observed in several BALB/c and ICR mice, reflecting the possibility of exacerbation of liver injury. These results suggest that the liver injury could be caused and sustained by a one-shot DTH reaction to picryl chloride. The chronicity of the biochemical and histopathological characteristics may be helpful in elucidating the mechanisms of chronic development of liver injury.

Animals↗
PubMed1997

Modulation of p53, WAF1/p21 and BCL-2 expression during retinoic acid-induced differentiation of NB4 promyelocytic cells.

The NB4 cell line, established from a patient with APL, carries the t(15; 17) and undergoes differentiation along the granulocytic pathway when exposed to retinoic acid (RA). The NB4 cell line was used as a model for exploring the expression of genes and proteins implicated in growth regulation, differentiation and apoptosis during treatment with RA. NB4 cells undergo a series of cytological and molecular alterations during RA treatment--Day 1: cell differentiation marked by an increase in CD11b is evident. Day 2: WAF1/p21 mRNA and then protein rise, though they drop 2 days later. Day 3: the percentage of cells in S phase begins to decrease and G1 arrest begins. Day 4: p53 mRNA level and then protein levels fall. Day 5: CD11b/BCL-2 double staining cells are markedly reduced. No signs of apoptosis were observed after up to 8 days of treatment with RA. These results demonstrate that NB4 cells treated with RA rapidly differentiate and arrest at G1 phase concurrent with p53-independent WAF1/p21 induction; in addition, phenotypic differentiation appears to commence before changes in cell cycle progression. An explanation for the decrease in p53 as well as the lack of apoptosis immediately after BCL-2 downregulation will require further study.

Antigens, CD↗
PubMed1997

The production of recombinant dengue virus E protein using Escherichia coli and Pichia pastoris.

The dengue virus envelope protein was expressed as a GST fusion protein using E. coli and P. pastoris as expression hosts. In E. coli the recombinant E protein is expressed initially as a soluble 81 kDa GST fusion protein. Treatment of the fusion protein with thrombin released a 55 kDa protein, which is the expected size for correctly processed, non-glycosylated recombinant E protein. The antiserum from animals immunised with this recombinant E protein was found to specifically recognise the dengue virus E protein in virus-infected cells, thus demonstrating the immunogenic nature of the recombinant E protein. This expression system allowed production of up to 2 mg of purified recombinant E protein from a 1 1 bacterial culture. In contrast, expression of this GST fusion protein in P. pastoris is associated with extensive proteolytic degradation of the recombinant E protein. However, this proteolytic degradation was not observed in the truncated E protein sequences which were expressed. One of these recombinant fusion proteins, GST E401 was secreted into the culture medium at levels of up to 100 microg/l of growth medium.

Animals↗
PubMed1997

Responses of plasma fibronectin to the changes of dietary protein levels in rats.

In this study, the plasma fibronectin was evaluated as a nutritional marker in protein- and protein-energy malnourished rats in comparison with plasma prealbumin, albumin, and total protein. The plasma fibronectin was determined by nephelometric assay based on the interaction of an antigen and antibody. The rats were subjected to three diets, containing 20, 5, and 0% casein, respectively, for 5 wk except in the last 2 wk, the rats on the 0% casein diet were re-fed on a 20% casein diet. The results showed that in the rats on a 5% casein diet (protein malnourished), the plasma fibronectin concentration rose significantly in the early stage and normalized thereafter. In the rats subjected to a 0% casein diet (protein-energy malnourished), the plasma fibronectin concentration did not decline quickly in response to protein depletion, compared with the plasma prealbumin, albumin, and total protein concentrations. Following the re-feeding of a 20% casein diet in the last 2 wk, the plasma fibronectin concentration was restored earlier than other plasma protein concentrations. No significant change in plasma fibronectin concentration was found in the rats receiving a 20% casein diet (control) over the 5 wk feeding period. It is concluded that plasma fibronectin may not be a suitable marker for protein or protein-energy malnutrition, though it is a sensitive index for nutritional rehabilitation.

Animals↗
PubMed1997

Multiplex sequencing of 1.5 Mb of the Mycobacterium leprae genome.

The nucleotide sequence of 1.5 Mb of genomic DNA from Mycobacterium leprae was determined using computer-assisted multiplex sequencing technology. This brings the 2.8-Mb M. leprae genome sequence to approximately 66% completion. The sequences, derived from 43 recombinant cosmids, contain 1046 putative protein-coding genes, 44 repetitive regions, 3 tRNAs, and 15 tRNAs. The gene density of one per 1.4 kb is slightly lower than that of Mycoplasma (1.2 kb). Of the protein coding genes, 44% have significant matches to genes with well-defined functions. Comparison of 1157 M. leprae and 1564 Mycobacterium tuberculosis proteins shows a complex mosaic of homologous genomic blocks with up to 22 adjacent proteins in conserved map order. Matches to known enzymatic, antigenic, membrane, cell wall, cell division, multidrug resistance, and virulence proteins suggest therapeutic and vaccine targets. Unusual features of the M. leprae genome include large polyketide synthase (pks) operons, inteins, and highly fragmented pseudogenes.

Amino Acid Sequence↗
PubMed1997

The Helicobacter pylori genome is modified at CATG by the product of hpyIM.

To understand mechanisms of DNA methylation in Helicobacter pylori, a human pathogen associated with peptic ulcer disease and gastric adenocarcinoma, we cloned a putative DNA methyltransferase gene, hpyIM. This gene contains a 990-bp open reading frame encoding a 329-amino-acid protein, M.HpyI. Sequence analysis revealed that M.HpyI was closely related to CATG-recognizing adenine DNA methyltransferases, including M.NlaIII in N. lactamica. hpyIM was present in all H. pylori strains tested. DNA from wild-type H. pylori strains was resistant to digestion by SphI and NlaIII, which recognize DNA at sites containing CATG, whereas their isogenic hpyIM mutants were susceptible, indicating lack of modification. Overexpression of hpyIM in Escherichia coli rendered DNA from these cells resistant to NlaIII digestion, confirming the role of hpyIM in modifying CATG sites. We conclude that hpyIM encodes a DNA methyltransferase, M.HpyI, that is well conserved among diverse H. pylori strains and that modifies H. pylori genomes at CATG sites.

Amino Acid Sequence↗
PubMed1997

The role of mast cells in atherosclerosis.

Mast cells are characterized by numerous granules released extracellularly in response to stimuli, e.g. IgE and complement. These cells are believed to be crucial in the development of certain inflammatory or immune-mediated diseases, such as allergy and dermatitis, and it has recently been demonstrated that a large number of mast cells are present in atherosclerotic lesions. Atherosclerosis bears several similarities to chronic inflammation, characterized by T cell and monocyte infiltration, immunoglobulin-complement deposition, and lipid accumulation. The presence of mast cells in atherosclerotic lesions could be significant because they can release large amounts of chemotactic agents, inflammation activators, and granule remnants, and they may be responsible for mononuclear cell recruitment and smooth muscle cell proliferation. Furthermore, granule remnants nonspecifically bind to low-density lipoproteins, which can be phagocytosed by macrophages to form foam cells, a major cellular component of the early stage of atherosclerotic lesions. Thus, further elucidation of the role of mast cells in quantitative studies could enhance our understanding of the mechanism of atherogenesis, and may lead to new therapeutic strategies for atherosclerosis.

Animals↗
PubMed1997

Salivary anti-hsp65 antibodies as a diagnostic marker for gingivitis and a possible link to atherosclerosis.

Levels of specific salivary IgA antibodies against mycobacterial heat shock protein (hsp) 65 are significantly increased in patients with gingivitis when compared to clinically healthy subjects. The process of identifying the hsp65 epitopes recognized by the salivary antibodies, binding to overlapping 15-mer-hsp65 peptides, was assessed. Time-resolved fluorescence immunoassays using 15-mer overlapping peptides spanning the whole hsp65 molecule revealed six distinct sequences recognized by anti-hsp65 IgA antibodies. Due to the high degree of sequence homology between mycobacterial hsp65, cognates of the hsp60 family of oral bacterial flora and human hsp60, these six epitopes may serve as cross-reactive autoantigens in certain circumstances in vivo and could incite an autoimmune response that contributes to the initiation of gingivitis.

Adult↗
PubMed1997

Activation of mitogen-activated protein kinases (ERK/JNK) and AP-1 transcription factor in rat carotid arteries after balloon injury.

Smooth muscle cell proliferation is a key event in neointimal formation after balloon angioplasty. The molecular signals that mediate this process have yet to be identified. Mitogen-activated protein (MAP) kinases are thought to play a pivotal role in transmitting transmembrane signals required for cell proliferation in vitro. The present studies were designed to investigate whether the signal transduction pathways of MAP kinases were involved in the development of restenosis in the injured arteries. Rat carotid arteries were isolated at various time points after balloon injury, and activities of MAP kinases, including extracellular signal-regulated kinases (ERK), and stress activated protein kinases (SAPK)/c-Jun N-terminal protein kinases (JNK), were determined in protein extracts of the vasculature using protein kinase assay and Western blot analysis. After balloon angioplasty, ERK2 and JNK1 activities in the vessel wall increased rapidly, reached a high level in 5 minutes and maintained for 1 hour. A sustained increase in ERK2 kinase activity was observed over the next 7 days in the arterial wall and 14 days in neointima after injury. In contrast, opposite and uninjured arteries did not show significant changes in these kinase activities. Concomitantly, Western blot analysis confirmed that the ERK2 kinase in the injured vessels was indeed activated or phosphorylated, showing a slowly migrating species of a 42-kDa protein containing phosphorylated tyrosine. Kinase activation is followed by an increase in c-fos and c-jun gene expression and enhanced activator protein 1 (AP-1) DNA-binding activity. Thus, balloon injury rapidly activates the MAP kinases in rat carotid arteries. These kinase activations may be crucial in mediating smooth muscle cell proliferation in response to vascular angioplasty.

Angioplasty, Balloon↗
PubMed1997

Epitope specificity of anti-heat shock protein 65/60 serum antibodies in atherosclerosis.

Levels of specific antibodies (Ab) against mycobacterial and human heat shock protein (hsp) 65/60 are increased in the sera of patients with atherosclerotic lesions and have been demonstrated to be capable of mediating endothelial cytotoxicity. To clarify the antigen epitopes recognized by these serum Abs, Ab binding to hsp65 deletion mutants (Dms), as well as to overlapping 15-mer and 8-mer hsp65 peptides, was assessed. Western blotting of hsp65 Dms indicated the presence of at least one epitope between amino acid (aa) residues 171 and 276, recognized by both high-titer sera and affinity-purified anti-hsp65/60 Ab. Fluorescence immunoassays using 53 15-mer peptides and Pin ELISA using 526 7-mer peptides demonstrated three distinct, conserved sequences with high affinity to high-titer sera and purified anti-hsp65/60 Ab. Two N-terminal sequences, aa 97-109 and aa 179-187, and one C-terminal sequence, aa 504-512, were identified. These three epitopes recognized by anti-hsp65/60 Ab may serve as autoantigens in certain circumstances in vivo. This phenomenon could contribute to the initiation of atherosclerosis by an autoimmune reaction.

Amino Acid Sequence↗
PubMed1997

Induction of mitogen-activated protein kinase phosphatase-1 during acute hypertension.

Recently, we demonstrated that elevated blood pressure activates mitogen-activated protein (MAP) kinases in rat aorta. Here we provide evidence that the vascular response to acute hypertension also includes induction of MAP kinase phosphatase-1 (MKP-1), which has been shown to function in the dephosphorylation and inactivation of MAP kinases. Restraint or immobilization stress, which leads to a rapid rise in blood pressure, resulted in a rapid and transient induction of MKP-1 mRNA followed by elevated MKP-1 protein expression in rat aorta. That the induction of MKP-1 by restraint was due to the rise in blood pressure was supported by the finding that several different hypertensive agents (phenylephrine, vasopressin, and angiotensin II) were likewise capable of eliciting the response, and sodium nitroprusside, a nonspecific vasodilator agent that prevented the acute rise in blood pressure in response to the hypertensive agents, abrogated MKP-1 mRNA induction. The in vivo effects could not be mimicked by treatment of cultured aortic smooth muscle cells with similar doses of the hypertensive agents. These findings support a role for MKP-1 in the in vivo regulation of MAP kinase activity during hemodynamic stress.

Acute Disease↗
PubMed1997

Co-expression of ICAM-1, VCAM-1, ELAM-1 and Hsp60 in human arterial and venous endothelial cells in response to cytokines and oxidized low-density lipoproteins.

T-cells and monocytes are the first cells infiltrating the arterial intima during the early stages of atherogenesis. Recently our laboratory has provided evidence that T-cells isolated from atherosclerotic intima reacts against heat shock protein 60 (Hsp60). Transmigration of activated T-cells into the intima is mediated by adhesion molecules (ICAM-1; VCAM-1; ELAM-1) expressed on activated endothelial cells. Here we studied the potential of cytokines (TNF-alpha, IFN-gamma, IL-1). Escherichia coli lipopolysaccharide (LPS), native and oxidized low-density lipoprotein (LDL; oxLDL) and high temperature to induce adhesion molecules as well as Hsp60 and Hsp70 expression in human endothelial cells (EC). On Northern blots, a strong signal for ICAM-1, VCAM-1 and ELAM-1 was detected after 4 h, which thereafter declined, but did not reach the basal level of untreated control cells. Heat shock induced the expression of Hsp60 and Hsp70 but not of adhesion molecules. EC were cultivated in serum-free medium, which led to the expression of adhesion molecule transcripts. Addition of LDL or oxLDL to these ECs did not alter the expression of these transcripts. The production of adhesion molecule proteins was analysed by flow cytometry. In human venous endothelial cells (HVEC) and human arterial endothelial cells (HAEC) ICAM-1 and VCAM-1 production was permanently highly induced, whereas the high level of ELAM-1 production at 4 h disappeared after 24 h. Furthermore, only HAEC, but not HVEC, produced ICAM-1, VCAM-1 and ELAM-1 after stress by moderately and highly oxLDL. LDL and oxLDL did not induce the production of Hsp60 and Hsp70. The present study demonstrates the co-expression of Hsp60 and adhesion molecules in arterial and venous EC in response to cytokine and LPS exposure, and that oxLDL is an efficient inducer of adhesion molecules in arterial EC and not in venous EC. These features provide the prerequisites for a cellular immune reaction against Hsp60 expressed by stressed EC in the initial stages of atherosclerosis.

Antigens, CD↗
PubMed1997

Potentiation of heat stress-induced hsp70 expression in vivo by aspirin.

Studies in cultured cells have demonstrated that non-steroidal anti-inflammatory agents can potentiate heat-induced hsp70 expression through activation of HSF1 to a DNA binding state. We investigated the influence of aspirin on hsp70 expression in intact rats subjected to heat stress. Rats were injected intraperitoneally either with aspirin (100 mg/kg) or vehicle alone, 60 min prior to their placement at 37 degrees C or room temperature for 30 min. hsp70 mRNA expression was analyzed in lung, liver and kidney isolated from animals assigned to one of four different treatment paradigms; untreated controls, heat, aspirin, and aspirin-plus-heat. Comparison of hsp70 expression in the treatment groups revealed that in all tissues examined, aspirin-plus-heat treatment resulted in 3-4 fold higher levels of hsp70 mRNA relative to those seen with heat treatment alone. Little or no hsp70 mRNA expression was detected in the unheated groups, regardless of aspirin treatment. In keeping with the mRNA expression, Hsp70 protein levels were also elevated in aspirin-plus-heat treated animals. Aspirin treatment did not alter hsp70 protein expression in the absence of heat. In contrast to in vitro observations, aspirin treatment in vivo did not alter HSF1 DNA binding properties. Core body temperature measurements revealed that aspirin pretreatment enhanced the rise in body temperature seen in response to heat treatment. This increased hyperthermic response to heat stress probably accounts for the potentiation of hsp70 expression observed in aspirin-plus-heat treated rats. Given the widespread use of aspirin in humans within a dose range comparable to that used here, our findings are likely to have important physiological consequences.

Animals↗
PubMed1997

[A study on the relationship between bone mineral content and the tissue calcium level in rats].

The relationship of bone mineral density (BMD) and bone mineral content (BMC) of femur bone with the tissue and blood calcium contents was studied with 98 Wistar rats (15-week old). The results indicated that the body length, body weight, bone width, BMC, BMC/weight, BMD/weight and BMD/length in male were markedly different from those in female animals. The BMD of alive rats was significantly correlated with the total calcium intake, length, weight and calcium retention rate (P < 0.05). BMC was significantly related to sex, length, weight, liver calcium content and total calcium intake. Multiple regression analysis indicated that the animal body length, weight, total calcium intake and calcium content in heart were positively correlated with the BMD of alive animals. The animal body length and plasma calcium content were positively correlated with BMD of separated bones after the animals were sacrificed. The present results indicated that the BMC and BMD of alive rats could reflect the calcium status and bone mineral accumulation in the body because of the significant correlation with the growth rate, calcium retention rate, muscle and plasma calcium contents, but not with the separated bone BMD or BMC.

Animals↗
PubMed1997

[Intracerebral grafting of ex vivo transgene muscle cells in rat model of parkinsonism].

The rat model with a unilateral 6-OHDA-induced lesion of the dopaminergic system was used for experimental study on gene therapy for Parkinson's disease (PD). The plasmid pCMVTH (6.04 kb) was constructed as a vector containing the gene of tyrosine hydroxylase (TH) and transferred into cultured primary muscle cells by lipofection ex vivo. After expression of TH was determined in vitro, the intracerebral grafting (ICG) of these genetically modified cells was made in the striatum of PD rat model. The results showed that TH-expressing muscle cells had a long-term survival in the brain and induced a marked decrease in abnormal locomotion and increase in striatal dopamine levels for rat model.

Animals↗
PubMed1997

[Mechanisms of thrombin induced proliferation and detachment of glomerular endothelial cells].

To clarify the mechanisms of thrombin contributing to the progression of glomerular diseases by injuring glomerular endothelial cells (GECs), we studied the effects of thrombin on GECs in vitro. Cell proliferation was detected with MTT incorporation, total plasminogen activator (PA) and tissue type PA (t-PA) activities were detected with fibrin plate and chromatogenic substrate methods and fibronectin was detected with ELISA as well as indirect immunofluore scence. 0.4-3.2 NIH U/ml thrombin promoted GEC proliferation significantly (P < 0.05). Thrombin promoted cell detachment, which can be inhibited by hirudin or aprotinin. Thrombin enhanced total PA and t-PA activities of GECs significantly (P < 0.01). Fibronectin in the supernatants of thrombin-stimulated GECs decreased significantly (P < 0.01) and in the extracellular compartment also decreased. The decrease was inhibited by hirudin and aprotinin. In conclusion, thrombin can induce GEC proliferation and GEC detachment. The latter is probably related to PA-mediated over-degradation of extracellular matrices such as fibronectin, which are needed for cell attachment.

Cell Division↗