Biomedical subjects

S Xiao

Publications and source records attributed to S Xiao.

At least 37 records · Page 2Linked to original sources

PubMed2001

Uremic levels of urea inhibit L-arginine transport in cultured endothelial cells.

Hypertension in end-stage renal disease (ESRD) may involve lack of endothelial nitric oxide (NO), as suggested by reduced total NO synthase (NOS) in dialysis patients. One reason might be due to substrate deficiency. To test the hypothesis that uremia is a state of intracellular L-arginine deficiency, uremic plasma was obtained from dialysis patients, and its effect was tested on arginine transport in cultured vascular endothelial cells. L-arginine transport (P < 0.01) was reduced in human dermal microvascular endothelial cells (HDMEC) incubated for 6 h with 20% uremic plasma from peritoneal dialysis and hemodialysis patients obtained immediately predialysis. Similar transport inhibition was seen with ESRD plasma in human glomerular capillary and bovine aortic endothelial cells. Hemodialysis partially reversed inhibition of L-arginine transport. HDMECs incubated for 6 h with synthetic media containing high (uremic) urea concentrations showed inhibition of L-arginine transport, but this was not competitive because acute exposure to urea had no impact on L-arginine transport. Over a 6-h period, urea-induced inhibition of L-arginine transport was not sufficient to inhibit NOS activity, but after 7 days NOS activity was reduced. These cellular findings suggest that substrate delivery may be lowered, thus reducing endothelial NOS activity and contributing to hypertension in ESRD patients.

Animals↗

PubMed2001

Uremic levels of BUN do not cause nitric oxide deficiency in rats with normal renal function.

In vitro, 7 days of high blood urea nitrogen (BUN) inhibits endothelial L-arginine transport and nitric oxide synthase (NOS) activity. The present study investigates whether 7 days of high BUN in vivo influences renal hemodynamics, blood pressure (BP), and/or the nitric oxide (NO) system. Normal rats were fed low-nitrate food containing 30% urea for 7 days, which increased BUN (15 +/- 1 to 69 +/- 4 mg/100 ml, P < 0.001). High BUN did not reduce 24-hour urinary nitrite/nitrate excretion (a measure of total NO production). Baseline BP and renal hemodynamics were unaffected by high BUN as were the pressor and renal vasoconstrictor responses to acute NOS inhibition with N(G)-nitro-L-arginine-methyl ester. In addition, high BUN had no impact on renal cortical L-arginine concentration, density of either endothelial NOS or neuronal NOS protein, or renal cortical NOS activity. NOS activity in the brain cerebellum was also unaffected. In conclusion, high BUN did not lead to vasoconstriction or NO deficiency in rats with normal renal function. Further studies are needed to evaluate the effect of high BUN on the NO system in rats with progressive renal functional insufficiency.

Animals↗

PubMed2001

Effects of estradiol and its metabolites on glomerular endothelial nitric oxide synthesis and mesangial cell growth.

Reduced nitric oxide synthesis by glomerular endothelial cells and increased proliferation of glomerular mesangial cells is associated with glomerular remodeling that leads to accelerated glomerulosclerosis. Estradiol induces nitric oxide synthesis and slows the progression of renal disease. Because the estradiol metabolites 2-hydroxyestradiol and 2-methoxyestradiol are more potent than estradiol in inhibiting growth of vascular smooth muscle cells, which are phenotypically similar to mesangial cells, we compared the effects of estradiol, 2-hydroxyestradiol, and 2-methoxyestradiol on growth of glomerular mesangial cells and on basal nitric oxide synthesis by glomerular endothelial cells. In human glomerular mesangial cells, estradiol and its metabolites concentration-dependently (1 nmol/L to 10 micromol/L) inhibited serum (2.5%)-induced DNA synthesis, cell proliferation, and collagen synthesis with the order of potency being 2-methoxyestradiol > 2-hydroxyestradiol > estradiol. ICI182780 (100 micromol/L, an estrogen receptor antagonist) blocked the growth inhibitory effects of estradiol but not 2-hydroxyestradiol or 2-methoxyestradiol. Treatment with estradiol, but not 2-hydroxyestradiol and 2-methoxyestradiol, induced nitric oxide synthesis (P<0.05, assayed by the formation of (3)H-L-citrulline from (3)H-L-arginine) in human glomerular endothelial cells, and these effects were blocked by ICI182780 and L-NMA (a nitric oxide synthesis inhibitor). In conclusion, estradiol may attenuate glomerulosclerosis by inducing nitric oxide synthesis via an estrogen receptor-dependent mechanism and by conversion to 2-hydroxyestradiol and 2-methoxyestradiol, which inhibit glomerular mesangial cell proliferation independent of estrogen receptors.

2-Methoxyestradiol↗

PubMed2001

Species-specific identification of human hookworms by PCR of the mitochondrial cytochrome oxidase I gene.

Significant differences in the life histories of the human hookworms Ancylostoma duodenale and Necator americanus necessitate their differentiation for epidemiological studies and the design of control programs. Current methods of identification require time-consuming, labor-intensive techniques. A polymerase chain reaction (PCR)-based method that enables rapid species identification is described. The mitochondrial cytochrome oxidase I genes of both species were sequenced, and species-specific primer sets were designed. The primers were used in PCR to amplify 585-bp fragments of the cytochrome oxidase gene from individual hookworm eggs, larvae, and adults. The technique was also able to identify mixed infections containing equal amounts of eggs from each species. The technique is rapid, technically simple, and sensitive and will permit the accurate identification of human hookworms in epidemiological field studies.

Ancylostoma↗

PubMed2001

Current progress in the development and use of artemether for chemoprophylaxis of major human schistosome parasites.

Human schistosomiasis, a chronic and debilitating parasitic disease of the tropics, is ranked second after malaria in terms of public health importance. At present, there is no vaccine available, and chemotherapy is the cornerstone of schistosomiasis control. Praziquantel is the drug of choice. Oxamniquine has become difficult to obtain and metrifonate has recently been withdrawn from the market. Rapid re-infection following treatment and concern about praziquantel resistance called for the search of novel drugs for prevention and cure of schistosomiasis. Significant progress has been made with artemether, the methyl ether of dihydroartemisinin, already widely used for the treatment of malaria. The present article reviews the literature that led to the development of artemether for chemoprophylaxis in schistosomiasis, and it summarises the experiences so far obtained with its use to control schistosomiasis in different endemic settings. Topics covered include an overview of the global burden of schistosomiasis and approaches for its control; the nature and features of artemisinin and related derivatives, initially discovered as antimalarials, other bioactivities, and their recent discovery of antischistosomal properties; a historic account disclosing the antischistosomal activity of artemether; in vivo assessment of drug susceptibility of different developmental stages of schistosome parasites; artemether-induced pathology evidenced by scanning and transmission electron microscopy; the possible mechanism of action; in vivo studies with combination therapy of artemether and praziquantel; results of randomised controlled clinical trials of oral artemether for the prevention of patent infection and morbidity; and, ultimately the translation of this knowledge into public health action in different endemic settings towards a more integrated approach of schistosomiasis control.

Animals↗

PubMed2001

[Study on the tissue culture and plant regeneration of Pogostemon cablin].

Root tips, leaf segments, stem segments with node and stem segments of Pogostemon cablin (Blanco) Benth. were cultured in vitro. The results indicated that leaf segments and stem segments with node were suitable for callus formation, the frequency of callus induction were over 87.0%. A optimal medium for callus induction was MT + BA 0.5 mg/L + NAA 0.2 mg/L. MT basal medium with BA 0.5-1.0 mg/L were effective to induce differentiation of callus. And at the MT basal medium, the regenerative shoots from Pogostemon cablin could form roots.

Culture Media↗

PubMed2001

[Bioactivity and test grafting of acellular dermal matrix containing fibroblasts].

OBJECTIVE: To investigate the bioactivity of acellular dermal matrix with fibroblasts and its role as dermal skeleton. METHODS: Human fibroblasts (HFs) were planted onto the surface of acellular dermal matrix (ADM) to form living dermal substitute. The IL -- 6, IL -- 8 and TGF contents in the supernatant of the culture of HF -- ADM were determined with ELISA method, and the secretion of hyaluronic acid and laminin from extracellular matrix was measured with RIA method. The speed of vascularization and the wound contracture rate were observed after the dermal substitute was grafted on the full skin loss wound of Balb/c-nu mice (nude mice). RESULTS: HFs grew very well after being planted onto ADM so as to form a single layer of cellular membrane. Many kinds of cytokines and extra cellular matrix components were secreted. Compared with simple acellular dermal grafting, the vascularization was accelerated, and the wound contracture rate decreased, after the living dermal substitute being grafted on the wound. CONCLUSION: The ADM seeded with HFs exhibited excellent bioactivity and might be an optimal dermal substitute.

Animals↗

PubMed2001

[Postlaryngectomy peristomal recurrence].

OBJECTIVE: To study the etiopathology, diagnosis and management of peristomal recurrence after laryngectomy, and the prevention of peristomal recurrence. METHODS: Retrospective analysis of clinical management and outcomes of 16 cases of peristomal recurrence. RESULTS: The subglottic extension of laryngeal cancer and peritracheal metastasis may result in peristomal recurrence. The stomal resection with mediastinal dissections and the use of the pectoralis major myocutaneous flap were done. The survival period of 11 cases surgically treated was longer than that of 5 cases irradiated or untreated. CONCLUSION: Surgical management would improve the survival, but overall prognosis is dismal and attention should be focused on prevention. It is evident that early diagnosis of stomal recurrences will yield good results.

Aged↗

PubMed2000

Eumetazoan fossils in terminal proterozoic phosphorites?

Phosphatic sedimentary rocks preserve a record of early animal life different from and complementary to that provided by Ediacaran fossils in terminal Proterozoic sandstones and shales. Phosphorites of the Doushantuo Formation, South China, contain eggs, egg cases, and stereoblastulae that document animals of unspecified phylogenetic position; small fossils containing putative spicules may specifically record the presence of sponges. Microfossils recently interpreted as the preserved gastrulae of cnidarian and bilaterian metazoans can alternatively be interpreted as conventional algal cysts and/or egg cases modified by diagenetic processes known to have had a pervasive influence on Doushantuo phosphorites. Regardless of this interpretation, evidence for Doushantuo eumetazoans is provided by millimeter-scale tubes that display tabulation and apical budding characteristic of some Cnidaria, especially the extinct tabulates. Like some Ediacaran remains, these small, benthic, colonial fossils may represent stem-group eumetazoans or stem-group cnidarians that lived in the late Proterozoic ocean.

Animals↗

PubMed2000

CD95 (Fas) ligand-expressing vesicles display antibody-mediated, FcR-dependent enhancement of cytotoxicity.

Bioactive Fas ligand (FasL)-expressing vesicles were generated (vesicle preparation, VP) from two cell lines overexpressing FasL. The effect of NOK-1 anti-FasL mAb (mouse IgG1) on the cytotoxicity of FasL VP against various targets was determined. At high concentrations (1-10 microg/ml), NOK-1 inhibited the cytotoxicity. By contrast, NOK-1 in the dose range of 1-100 ng/ml significantly enhanced cytotoxicity against the FcR(+) LB27.4, M59, and LF(+) targets, but not the FcR(-) Jurkat and K31H28 hybridoma T cell targets. The ability to enhance FasL VP-mediated cytotoxicity could be blocked by the FcR-specific mAb 2.4G2. Enhancement was also observed with FcR(+) A20 B lymphoma but not with the FcR(-) A20 variant. Enhancement of FasL VP cytotoxicity was observed with five IgG anti-FasL mAbs, but not with an IgM anti-FasL mAb. Inhibition was observed with high doses of all mAb except the IgG anti-FasL mAb G247-4, which is specific to a segment outside the FasL binding site. Interestingly, under identical conditions but in the presence of 2.4G2, G247-4 inhibited the cytotoxicity of FasL VP. In addition, G247-4 inhibited the FasL VP-mediated killing of FcR(-) Jurkat. The data demonstrate that FasL-expressing bioactive vesicles display a property heretofore unknown in bioactive agents that express FasL-mediated cytotoxicity. The mechanism of the Ab-mediated, FcR-dependent enhancement of cytotoxicity of bioactive vesicles and its physiological significance are discussed.

Adjuvants, Immunologic↗

PubMed2000

Refinement of the locus for autosomal dominant hereditary gingival fibromatosis (GINGF) to a 3.8-cM region on 2p21.

Hereditary gingival fibromatosis (HGF, MIM 135300; approved gene symbol GINGF) is an oral disease characterized by enlargement of gingiva. Recently, a locus for autosomal dominant HGF has been mapped to an 11-cM region on chromosome 2p21. In the current investigation, we genotyped four Chinese HGF families using polymorphic microsatellite markers on 2p21. The HOMOG test provided evidence for genetic homogeneity, with evidence for linkage in four families (heterogeneity versus homogeneity test HOMOG, chi(2) = 0. 00). A cumulative maximum two-point lod score of 5.04 was produced with marker D2S390 at a recombination frequency of θ = 0 in the four linked families. Haplotype analysis localized the hereditary gingival fibromatosis locus within the region defined by D2S352 and D2S2163. This region overlaps by 3.8 cM with the previously reported HGF region. Single-strand conformation polymorphism and sequence analysis of the coding region of cytochrome P450 1B1 (CYP1B1) excluded it as a likely candidate gene.

Aryl Hydrocarbon Hydroxylases↗

PubMed2000

PLAG1 fusion oncogenes in lipoblastoma.

Lipoblastomas are pediatric neoplasms resulting from transformation of adipocytes. These benign tumors are typically composed of adipose cells in different stages of maturation within a variably myxoid matrix, and they contain clonal rearrangements of chromosome band 8q12. Because lipoblastomas resemble embryonic adipose tissue, characterization of their transforming mechanisms might reveal biological pathways in physiological adipogenesis. Herein, we demonstrate that lipoblastoma chromosome 8q12 rearrangements bring about promoter-swapping events in the PLAG1 oncqgene. We show that the hyaluronic acid synthase 2 (HAS2) or collagen 1 alpha 2 (COL1A2) gene promoter regions are fused to the entire PLAG1 coding sequence in each of four lipoblastomas. PLAG1 is a developmentally regulated zinc finger gene whose tumorigenic function has been shown previously only in epithelial salivary gland cells. Our findings reveal that PLAG1 activation, presumably resulting from transcriptional up-regulation, is a central oncogenic event in lipoblastoma.

Adipose Tissue↗

PubMed2000

ZNF198-FGFR1 transforming activity depends on a novel proline-rich ZNF198 oligomerization domain.

An acquired chromosomal translocation, t(8;13)(p11;q11-12), observed in a distinctive type of stem cell leukemia/lymphoma syndrome, leads to the fusion of the 5' portion of ZNF198 and the 3' portion of FGFR1. ZNF198-FGFR1 fusion transcripts encode 4 to 10 zinc fingers, a proline-rich region, and the intracellular portion of the FGFR1 (fibroblast growth factor receptor 1) receptor tyrosine kinase. We demonstrate that the ZNF198 proline-rich region constitutes a novel self-association domain. When fused to the intracellular domain of FGFR1, the ZNF198 proline-rich region is sufficient to cause oligomerization, FGFR1 tyrosine kinase activation, and transformation of Ba/F3 cells to IL-3 independent growth. (Blood. 2000;96:699-704)

Animals↗

PubMed2000

Tegumental changes in 21-day-old Schistosoma mansoni harboured in mice treated with artemether.

Alterations in the tegument of 21-day-old Schistosoma mansoni, caused by artemether administered to the infected mice, were studied using scanning electron microscopy (SEM). Mice were infected with S. mansoni cercariae, and after 21 days a single dose of artemether (400 mg/kg) was administered intragastrically. After 24, 72 h and 7 days groups of three mice were killed and the schistosomules collected by perfusion, fixed and processed routinely, and examined by SEM. After 24 h, all male and female worms examined showed alterations in the tegument, characterised by swelling, vesiculation and fusion of tegumental ridges; peeling, erosion and collapse of damaged tegumental surface, and also destruction of the oral sucker and acetabulum. After 72 h, severe damage to the tegument was seen, usually including extensive peeling, swelling and vesiculation, and host leukocytes were adhered to the damaged surface. Some worms were surrounded by clusters of host leukocytes or had even disintegrated. Seven days after treatment, some schistosomules still showed severe tegumental damage, but in some cases the damage was less than at earlier times, which suggested that those schistosomules that had survived were beginning to recover. The ability of artemether to cause severe damage to the tegument correlates with its high efficacy in killing 21-day-old schistosomules.

Administration, Oral↗

PubMed2000

Oral artemether for prevention of Schistosoma mansoni infection: randomised controlled trial.

BACKGROUND: Chemotherapy with praziquantel is the current strategy of choice to control schistosomiasis. However, in view of concern about praziquantel tolerance or resistance, new drugs are needed. Artemether, a derivative of the antimalarial drug artemisinin, kills immature schistosomes of Schistosoma japonicum, and reduces the incidence of infection in field trials. Laboratory studies have also showed activity by this drug against S. mansoni. We report a randomised double-blind placebo-controlled clinical trial of artemether to prevent S. mansoni infection. METHODS: The trial was done in an area of western Côte d'Ivoire endemic for S. mansoni. 354 schoolchildren were enrolled. Stool specimens were screened over four consecutive days, followed by two mass treatments with praziquantel 4 weeks apart. All S. mansoni negative children were randomly assigned to placebo (n=151) or artemether 6 mg/kg (n=138) orally six times once every 3 weeks. Adverse events were assessed 24 h after treatment. Perceived illness episodes were recorded once a week by interviewing the children with a standardised questionnaire. 3 weeks after the final medication S. mansoni infections were assessed by screening stool samples. Blood samples were examined for Plasmodium falciparum before the first and after the last artemether treatment. FINDINGS: Oral artemether showed no adverse reactions. The group that received artemether had a significantly lower incidence of S. mansoni infection (31/128 versus 68/140, relative risk: 0.50 [95% CI 0.35-0.71], p=0.00006). The geometric mean egg output among positive children in the artemether group was significantly lower than in placebo recipients (19 vs 32 eggs/g stool, p=0.017). There was also a significant reduction in the prevalence of P. falciparum. INTERPRETATION: Oral artemether is safe and shows a prophylatic effect against S. mansoni. The use of artemether may be recommended in appropriated situations as an additional tool for more effective schistosomiasis control measures. However the application needs to be carefully assessed especially in view of the concern that it could select for resistant plasmodia.

Administration, Oral↗

PubMed2000

Role of activator protein-1 in TCR-mediated regulation of the murine fasl promoter.

The present study demonstrates that transcription factor interactions are important in regulating the murine fasl promoter following TCR-mediated activation. We used DNase I-footprinting, EMSAs, and transient transfection assays to identify the minimal TCR signal-responsive region within the fasl promoter. This region contains the previously identified binding sites for NF-kappaB and Egr and the AP-1 site identified in this study. We found that TCR signaling induces AP-1 binding to this site and regulates the fasl promoter function in a fashion dependent on NF-kappaB binding. However, mutation in the AP-1 site alone did not show a significant effect on the promoter function. The data suggest that the minimal promoter required at least two transcription factors to function.

Animals↗

PubMed2000

Clinical and CT histological diagnosis of orbital tumors.

The clinical manifestation and characteristics of CT image of 117 cases of orbital tumors in our hospital were investigated. The hemangioma had the highest incidence, and the less common tumors were, in sequence of incidence, pseudotumor, dermoid cysts, neurilemmoma, polymorphous adenoma and meningioma. The sensitivity in diagnosis of orbital tumor by CT was 93.3%. The coincidence of CT histological diagnosis with pathology were 83.3%, 82.6% and 71.4% for dermoid cysts, hemangioma, and pseudotumor respectively, but the general coincidence of CT histological diagnosis with pathology was only 67.8%. When CT was combined with ultrasound, cytological examination and clinical manifestations, the accuracy of histological diagnosis could be improved to 83.3%.

Dermoid Cyst↗

PubMed2000

TPM3-ALK and TPM4-ALK oncogenes in inflammatory myofibroblastic tumors.

Inflammatory myofibroblastic tumors (IMTs) are neoplastic mesenchymal proliferations featuring an inflammatory infiltrate composed primarily of lymphocytes and plasma cells. The myofibroblastic cells in some IMTs contain chromosomal rearrangements involving the ALK receptor tyrosine-kinase locus region (chromosome band 2p23). ALK-which is normally restricted in its expression to neural tissues-is expressed strikingly in the IMT cells with 2p23 rearrangements. We now report a recurrent oncogenic mechanism, in IMTs, in which tropomyosin (TPM) N-terminal coiled-coil domains are fused to the ALK C-terminal kinase domain. We have cloned two ALK fusion genes, TPM4-ALK and TPM3-ALK, which encode approximately 95-kd fusion oncoproteins characterized by constitutive kinase activity and tyrosylphosphorylation. Immunohistochemical and molecular correlations, in other IMTs, implicate non-TPM ALK oncoproteins that are predominantly cytoplasmic or pre- dominantly nuclear, presumably depending on the subcellular localization of the ALK fusion partner. Notably, a TPM3-ALK oncogene was reported recently in anaplastic lymphoma, and TPM3-ALK is thereby the first known fusion oncogene that transforms, in vivo, both mesenchymal and lymphoid human cell lineages.

Adult↗