Biomedical subjects

X Feng

Publications and source records attributed to X Feng.

At least 19 recordsLinked to original sources

PubMed2006

Carbon sinks and sources in China's forests during 1901-2001.

This paper reports the annual carbon (C) balance of China's forests during 1901-2001 estimated using the Integrated Terrestrial Ecosystem C-budget model (InTEC). Annual carbon source and sink distributions are simulated for the same period using various spatial datasets including land cover and leaf area index (LAI) obtained from remote sensing, soil texture, climate, forest age, and nitrogen deposition. During 1901-1949, China's forests were a source of 21.0+/-7.8 Tg C yr(-1) due to disturbances (human activities). Its size increased to 122.3+/-25.3 Tg C yr(-1) during 1950-1987 due to intensified human activities in the late 1950s, early 1960s, 1970s and early 1980s. The forests became large sinks of 176.7+/-44.8 Tg C yr(-1) during 1988-2001, owing to large-scale plantation and forest regrowth in previously disturbed areas as well as growth stimulation by nondisturbance factors such as climatic warming, atmospheric CO(2) fertilization, and N deposition. From 1901 to 2001, China's forests were a small carbon source of 3.32 Pg C, about 32.9+/-22.3 Tg C yr(-1). The overall C balance in biomass from InTEC generally agrees with previous results derived from forest inventories of China's forests. InTEC results also include C stock variation in soils and are therefore more comprehensive than previous results. The uncertainty in InTEC results is still large, but it can be reduced if a detailed forest age map becomes available.

Agriculture↗

PubMed2006

Csk-binding protein (Cbp) negatively regulates epidermal growth factor-induced cell transformation by controlling Src activation.

Epidermal growth factor receptor (EGFR) and Src tyrosine kinase cooperate in regulating EGFR-mediated cell signaling and promoting cell transformation and tumorigenesis in pathological conditions. Activation of Src is tightly regulated by the C-terminal Src kinase (Csk). The Csk-binding protein (Cbp) is a ubiquitously expressed transmembrane protein. Its functions include suppression of T-cell receptor activation through recruiting Csk and inhibiting Src family kinase (SFK). However, a potential role of Cbp in EGF-induced cell activities has not been investigated. Here, we report that EGF-stimulation-induced Cbp tyrosine phosphorylation followed by Cbp-Csk association, in a SFK-dependent manner. Expression of wild-type (wt) Cbp remarkably suppressed EGF-induced activation of Src, ERK1/2, and Akt-1 enzymes, and NIH3T3 cell transformation, as well as colony formation of a breast cancer cell line (MDA-MB-468) in soft agar. In contrast, expression of CbpY317F or knockdown endogenous Cbp in NIH3T3 cells by RNA interference significantly enhanced EGF-induced activation of these enzymes and cell transformation. In addition, overexpression of multiple receptor tyrosine kinases (RTKs)-induced Cbp tyrosine phosphorylation. These results demonstrate that Cbp functions as a negative regulator of cell transformation and tumor cell growth through downregulation of Src activation, suggesting that Cbp might be broadly involved in RTKs-activated signaling pathways and tumorigenesis.

Animals↗

PubMed2006

Gain of 1q25-32, 12q23-24.3, and 17q12-22 facilitates tumorigenesis and progression of human squamous cell lung cancer.

To explore the genetic changes involved in the stepwise development of lung cancer, we have determined the genetic events associated with the histological progression from normal bronchial epithelium to squamous cell carcinoma. Comparative genomic hybridization was used to identify chromosomal imbalances in 54 microdissected samples, including squamous metaplasia, dysplasia, carcinoma in situ, and invasive tumour derived from 23 patients with squamous cell carcinoma of the lung. Histopathological progression was accompanied by an increased number of chromosomal abnormalities. Gains of 1q25-32, 12q23-24.3, and 17q12-22, in particular, were detected at high frequencies in both carcinoma in situ and invasive tumours and were found more often in the cases with lymph node metastases than in those without. Our previous expression profiling of squamous cell carcinomas had identified overexpression of laminin5 gamma2, a gene located at 1q25-31. Therefore, this was investigated at the protein level by immunohistochemical analysis in 336 samples of squamous cell carcinoma of the lung. Consistent with the genomic data for this region, the expression level of laminin5 gamma2 was higher in the primary tumours with lymph node metastases than in tumours without metastases (p = 0.012). These data suggest that gains of genes from 1q25-32, 12q23-24.3, and 17q12-22 facilitate tumorigenesis and progression of squamous cell carcinoma of the lung, and may serve as potential predictors for this disease.

Aged↗

PubMed2006

Photolytic degradation of organic azo dye in aqueous solution using Xe-excimer lamp.

The photodegradation of organic azo dye C.I. Food Yellow 4 (FY-4) in aqueous solution was achieved, without the addition of oxidants, by 172 nm vacuum ultraviolet (VUV) radiation emitted from the planar Xe-excimer lamp. The degradation was mainly attributed to the impact of HO radicals produced by water absorbing VUV radiation. The dye decolorization followed pseudo-first order kinetics. The initial quantum yields of FY-4 decolorization in O2-saturated solution and N2-saturated solution were respectively 0.151 +/- 0.003 and 0.103 +/- 0.002. Dissolved oxygen in the solution contributed to the increase of the decolorization rate and chemical oxygen demand (COD) removal rate while KCI added as HO radical scavenger decreased the efficiency of the decolorization and COD removal. It was found from the change of the UV-Vis spectra that the degradation of FY-4 was accompanied by both the cleavage of chromophoric group and the opening of aromatic ring. Major intermediates detected were aromatic compounds, some low molecular weight by-products and several organic acids and inorganic ions.

Azo Compounds↗

PubMed2006

Synthetic oligosaccharide stimulates and stabilizes angiogenesis: structure-function relationships and potential mechanisms.

To determine the proangiogenesis effect of series of saccharides and a synthetic oligosaccharide and potential mechanisms, an in vitro 3-dimensional endothelial cell sprouting (3D-ECS) assay and the chick chorioallantoic membrane (CAM) model were used. We demonstrated that a sulfated oligosaccharide significantly promotes the endothelial capillary network initiated by vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (b-FGF). Furthermore, although the capillary network initiated by VEGF and b-FGF lasts no more than 7 days, addition of a sulfated oligosaccharide significantly amplifies angiogenesis and stabilizes the capillary network of new blood vessels. In the CAM model, sulfated oligosaccharide also stimulated angiogenesis. In both the CAM and the 3D-ECS assay, structure-function studies reveal that increased saccharide chain length up to the hexa- to decasaccharide show optimal proangiogenesis efficacy. In addition, the sulfation and molecular shape (branched vs linear) of oligosaccharide are important for sustained proangiogenesis efficacy. Data indicate that chemically defined synthetic oligosaccharides can play an important role in regulation of capillary structure and stability, which may contribute to future advances in therapeutic angiogenesis. The proangiogenesis efficacy of an oligosaccharide is mediated via integrin alphavbeta3 and involves mitogen-activated protein kinase signaling mechanisms.

Animals↗

PubMed2006

Influence of hydroxyethyl starch 130/0.4 in pulmonary neutrophil recruitment and acute lung injury during polymicrobial sepsis in rats.

BACKGROUND: Acute lung injury (ALI) is a progressive syndrome associated with significant mortality in sepsis patients. Neutrophils are key cells in the inflammatory response that characterizes ALI. This study was designed to explore the effects of hydroxyethyl starch (HES) 130/0.4 (a novel plasma substitute) on pulmonary neutrophil recruitment and associated ALI in a rat sepsis model induced by cecal ligation and puncture (CLP). METHODS: Animals were randomly assigned to six groups [saline control; CLP and saline; CLP and HES (7.5, 15 and 30 ml/kg); and HES control], subjected to CLP and infused with or without HES 130/0.4 4 h after CLP. Six hours later, the pulmonary capillary permeability (PCP), myeloperoxidase (MPO) activity, lung histological changes, tumor necrosis factor-alpha, interleukin-1beta and cytokine-induced neutrophil chemoattractant levels, P-selectin mRNA expression and nuclear factor-kappa B (NF-kappaB) activation were measured. RESULTS: Resuscitation with HES 130/0.4 significantly attenuated the CLP-induced increase in PCP, MPO activity, cytokine/chemokine levels, mRNA expression of P-selectin and NF-kappaB activation, all of which are involved in the recruitment of neutrophils. Groups receiving the higher doses of HES 130/0.4 (15 and 30 ml/kg) were more adequately resuscitated. CONCLUSION: HES 130/0.4 can inhibit CLP-induced neutrophil recruitment and subsequent ALI by attenuating cytokines/chemokines, adhesion molecule-mediated inflammation and NF-kappaB activation.

Animals↗

PubMed2006

Cyclooxygenase-2 plays an essential part in cardioprotection of delayed phase of recombinant human erythropoietin preconditioning in rats.

AIMS: To study the cardioprotection of recombinant human erythropoietin (rhEPO) preconditioning (EPC) and to investigate the role and possible mechanism of cyclooxygenase (COX)-2 in the delayed phase of EPC. METHODS: In phase 1, myocardial ischaemia reperfusion (I-R) rat model was established by 30 minutes ligation of left descending coronary and three hours of reperfusion. Rats were given 0.9% saline solution or rhEPO 24 hours before I-R protocol. COX-2 selective inhibitor celecoxib was given for further investigation of the cardioprotection of EPC. At the end of I-R protocol, infarct sizes were measured and ultrastructural organisations were studied. In phase 2, myocardial COX-2 mRNA expressions and prostaglandins (PGs) contents were studied in different groups after euthanasia. RESULTS: It was found that EPC could elicit potent cardioprotection against I-R injury, shown by reduction of infarct size and improvement of ultrastructural organisation; whereas administration of celecoxib resulted in complete loss of this protection. EPC resulted in robust increase in COX-2 mRNA and PGs levels that were also abrogated by celecoxib. CONCLUSIONS: COX-2 plays an essential part in cardioprotection of the delayed phase of EPC in rats, which might be related to actions of PGE(2) or PGI(2), or both.

Animals↗

PubMed2006

Pro-angiogenesis action of thyroid hormone and analogs in a three-dimensional in vitro microvascular endothelial sprouting model.

AIM: Our laboratory has recently demonstrated the pro-angiogenesis effects of thyroid hormone in the chick chorioallantoic membrane model. METHODS: Generation of new blood vessels from existing vessels was promoted two- to three-fold by either L-thyroxine (T4) or 3,5,3'-triiodo-L-thyronine (T3) at total hormone concentrations of T7-T9 M. RESULTS: T4-agarose, a formulation of thyroid hormone that does not cross the cell membrane, produced a potent pro-angiogenesis effect comparable to that obtained with T3 or T4. In the present investigation, T3, T4, T4-agarose, and basic fibroblast growth factor, each added to vascular endothelial growth factor, produced comparable pro-angiogenesis effects in the in vitro three-dimensional human microvascular endothelial sprouting model. The pro-angiogenesis effect of the thyroid hormone analogs was blocked by PD 98059, an inhibitor of the mitogen-activated protein kinase (MAPK; ERK1/2) signal transduction cascade. A specific avb3 integrin antagonist (XT199) also inhibited the pro-angiogenesis effect of either thyroid hormone analogs or T4-agarose. Tetrac, a thyroid hormone analog that blocks cell surface-initiated actions of T4 and T3, inhibited the pro-angiogenesis response of thyroid hormone. CONCLUSIONS: T4, T3, and T4-agarose are pro-angiogenic in the three-dimensional human microvascular endothelial sprouting model, an action that is initiated at the plasma membrane, involves avb3 integrin receptors, and is MAPK-dependent.

Cells, Cultured↗

PubMed2004

Metabolic activation of AMP kinase in vascular smooth muscle.

AMP-activated kinase (AMPK) is a highly conserved heterotrimeric kinase that functions as a metabolic master switch to coordinate cellular enzymes involved in carbohydrate and fat metabolism that regulate ATP conservation and synthesis. AMPK is activated by conditions that increase AMP-to-ATP ratio, such as exercise and metabolic stress. In the present study, we probed whether AMPK was expressed in vascular smooth muscle and would be activated by metabolic stress. Endothelium-denuded porcine carotid artery segments were metabolically challenged with 2-deoxyglucose (10 mM) plus N(2) (N(2)-2DG). These vessels exhibited a rapid increase in AMPK activity by 1 min that was near maximal by 20 min. AMPK inactivation on return to normal physiological saline was approximately 50% in 1 min and fully recovered by 5 min. Immunoprecipitation of the alpha(1)- and alpha(2)-catalytic subunit followed by immunoblot analysis for [P]Thr(172)-AMPK indicates that alpha(1)-AMPK accounts for all activity. Little if any alpha(2)-AMPK was detected in carotid smooth muscle. AMPK activity was not increased by contractile agonist (endothelin-1) or by the reported AMPK activators 5-aminoimidazole-4-carboxamide ribofuranoside (2 mM), metformin (2 mM), or phenformin (0.2 mM). AMPK activation by N(2)-2DG was associated with a rapid and pronounced reduction in endothelin-induced force and reduced phosphorylation of Akt and Erk 1/2. These data demonstrate that AMPK expression differs in vascular smooth muscle compared with striated muscles and that activation and inactivation after metabolic stress occur rapidly and are associated with signaling pathways that may regulate smooth-muscle contraction.

Adenylate Kinase↗

PubMed2004

Gap junctions are required for trophoblast proliferation in early human placental development.

Little is known about the role of gap junctional intercellular communication (GJIC) in human trophoblast differentiation, particularly during the formation of extravillous trophoblast (EVT) cell columns and their subsequent differentiation into invasive cells. We have identified transcripts for five connexin gap junction proteins in the early human placenta (Cx32, Cx37, Cx40, Cx43 and Cx45). Of these, Cx40 and Cx45 proteins immunolocalize to EVT in anchoring cell columns. Cx40 expression is prominent in the anchoring column throughout the first trimester of pregnancy (6-14 weeks gestation). We used first trimester placental villous explant cultures to determine the functional significance of the inhibition of GJIC in EVT cell proliferation and differentiation using two known GJIC inhibitors, carbenoxolone (CBX) and heptanol. The morphology of EVT outgrowths changed dramatically upon GJIC-blockade, from compact and organized outgrowths into a scattered group of rounded individual trophoblast cells, reminiscent of an early invasive phenotype. Furthermore, the inhibition of GJIC in placental explants by CBX or heptanol induced a switch away from the proliferative and towards an invasive EVT phenotype, as evident from (a) the loss of the proliferation marker Ki67 and (b) an increase in the invasive marker alpha1 integrin. We also utilized antisense oligonucleotides to inhibit Cx40 protein expression in placental explants. Cx40 antisense treatment also resulted in the abolishment of outgrowth EVT cell proliferation (as determined by Ki67 immunostaining). Together, these results suggest that gap junctions composed particularly of Cx40 channels are required for the proliferation of EVT cells in anchoring cell columns, and that a loss of GJIC contributes to differentiation to the invasive EVT phenotype.

Carbenoxolone↗

PubMed2004

Expansion and activation of minor histocompatibility antigen HY-specific T cells associated with graft-versus-leukemia response.

The immune system of females is capable of recognizing and reacting against the male-specific minor histocompatibility antigen (mHA), HY. Thus, cytotoxic T-lymphocytes (CTLs) recognizing this antigen may be useful in eradicating leukemic cells of a male patient if they can be generated in vivo or in vitro from a human leukocyte antigen (HLA)-identical female donor. The HLA-A*0201-restricted HY antigen, FIDSYICQV, is a male-specific mHA. Using HLA-A2/HY peptide tetrameric complexes, we reveal a close association between the emergence of HY peptide-specific CD8(+) T cells in peripheral blood and molecular remission of relapsed BCR/ABL(+) chronic myelogenous leukemia in lymphoid blast crisis in a patient who underwent female-to-male transplantation. Assessment of intracellular cytokine levels identified T cells that produce interferon-gamma in response to the HY peptide during the presence of HY tetramer-positive T cells. These results indicate that transplant with allogeneic HY-specific CTLs has therapeutic potential for relapsed leukemia, and that expansion of such T cells may be involved in the development of a graft-versus-leukemia response against lymphoblastic leukemia cells.

Adolescent↗

PubMed2004

Anesthetic management for separation of craniopagus twins.

We report the anesthetic management of a case of separation of craniopagus twins with unbalanced cross circulation and one twin with renal dysfunction. After intravenous induction, anesthesia was maintained with isoflurane inhalation and propofol infusion. Twin A survived but Twin B died after the surgery. The anesthetic problems during the operation are discussed.

Anesthesia↗

PubMed2003

Agrobacterium-mediated large-scale transformation of wheat (Triticum aestivum L.) using glyphosate selection.

An Agrobacterium-mediated transformation system with glyphosate selection has been developed for the large-scale production of transgenic plants. The system uses 4-day precultured immature embryos as explants. A total of 30 vectors containing the 5-enol-pyruvylshikimate-3-phosphate synthase gene from Agrobacterium strain CP4 (aroA:CP4), which confers resistance to glyphosate, were introduced into wheat using this system. The aroA:CP4 gene served two roles in this study-selectable marker and gene of interest. More than 3,000 transgenic events were produced with an average transformation efficiency of 4.4%. The entire process from isolation of immature embryos to production of transgenic plantlets was 50-80 days. Transgenic events were evaluated over several generations based on genetic, agronomic and molecular criteria. Forty-six percent of the transgenic events fit a 3:1 segregation ratio. Molecular analysis confirmed that four of six lead transgenic events selected from Agrobacterium transformation contained a single insert and a single copy of the transgene. Stable expression of theAROA:CP4 gene was confirmed by ELISA through nine generations. A comparison of Agrobacterium-mediated transformation to a particle bombardment system demonstrated that the Agrobacterium system is reproducible, has a higher transformation efficiency with glyphosate selection and produces higher quality transgenic events in wheat. One of the lead events from this study, no. 33391, has been identified as a Roundup Ready wheat commercial candidate.

Biolistics↗

PubMed2003

Physiological and molecular effects of Apo2L/TRAIL and cisplatin in ovarian carcinoma cell lines.

Combining of tumor necrosis factor-related apoptosis-inducing ligand (Apo2L/TRAIL) with a chemotherapeutic drug, cisplatin, in ovarian carcinoma cell lines exerted potent anti-tumor effects that exceeded the effects of each drug alone. In order to investigate mechanisms of anti-tumor activity of cisplatin/Apo2L/TRAIL combination, we assessed in detail the molecular effects of cisplatin and Apo2L/TRAIL-activated cell death in two ovarian carcinoma cell lines, OVCAR3 and SKOV3, using cDNA array hybridization, Western blot and flow cytometry. We observed differential induction of apoptosis-related molecules by cisplatin and Apo2L/TRAIL. Cisplatin upregulated the expression of both death and decoy TRAIL receptors, as well as of TRAF5 and -6, downregulated the anti-apoptotic proteins, Bcl-2, and induced activation of caspases-3, -8 and -9. Apo2L/TRAIL induced the expression of pro-apoptotic proteins, Bad and Bax; downregulated the anti-apoptotic proteins, Bcl-2 and Bcl-xL; and activated caspases-3, -7, -8, -9 and -10. Cisplatin/Apo2L/TRAIL combination resulted in further downregulation of expression of anti-apoptotic proteins, Bcl-2 and Bcl-xL, as well as an increase in mitochondrial permeability transition and activation of caspases-3, -8, and -10. These data demonstrate positive cooperation of cisplatin and Apo2L/TRAIL and emphasize the potential clinical usefulness of cisplatin/Apo2L/TRAIL combination therapy.

Antineoplastic Agents↗

PubMed2003

Gene expression profile of cardiomyocytes in hypertrophic heart induced by continuous norepinephrine infusion in the rats.

Catecholamines play an important role in the development of cardiac hypertrophy. To observe cardiomyocyte-specific gene expression changes induced by catecholamines in vivo, left ventricular cardiomyocytes were isolated from male Sprague-Dawley rats after continuous infusion of norepinephrine (NE; 0.2 mg/kg per hour intravenously) for 0.5, 1, 2, 3 and 7 days. The gene expression profiles of these cells during different NE infusion stages were assessed by using a cDNA microarray, and the microarray data were further analyzed by a clustering method. Cardiac hypertrophy was induced upon continuous NE infusion, with the peak at 3 days. Meanwhile, manifest changes in gene expression profile within cardiomyocytes over the time course were revealed, most of the genes never having been reported to be involved in cardiac hypertrophy. The number of genes displaying differential expression also peaked at the middle stage of infusion (2-3 days), and the majority of the signaling molecules were found differentially expressed mainly at this stage, including phosphatidylinositol 3-kinase, calcium/calmodulin-dependent protein kinase II and non-receptor tyrosine kinases, etc. The tumor suppressor p53 was found up-regulated at very early (0.5 days) and late stages (7 days) of NE infusion. Self-organization clustering analysis revealed subsets of coordinate regulated genes. One set consisted of several enzymes involved in energy metabolism, including carnitine octanoyltransferase, ATP synthase subunit c, pancreatic lipase and glycogen phosphorylase, possessing a similar expression pattern with a rapidly elevated expression level at the early stage of NE infusion. This is the first study to provide transcriptional information for cardiomyocytes, a single cell type, in the heart during the development of cardiac hypertrophy in vivo, and may provide accurate clues to elaborate hypotheses about the evolution of this pathology.

Animals↗

PubMed2002

Fully human antibodies to MCAM/MUC18 inhibit tumor growth and metastasis of human melanoma.

MCAM/MUC18 expression correlates with tumor thickness and metastatic potential of human melanoma cells in nude mice. Moreover, ectopic expression of MUC18 in primary cutaneous melanoma cells leads to increased tumor growth and metastasis in vivo. Here we tested the effect of a fully human anti-MUC18 antibody, ABX-MA1, on angiogenesis, tumor growth, and metastasis. ABX-MA1 had no effect on melanoma cell proliferation rate in vitro. However, when cells of the metastatic melanoma lines A375SM and WM2664 (which express high levels of MUC18) were injected s.c. into nude mice and treated with ABX-MA1 (100 micro g, weekly, i.p. for 5 weeks), tumor growth was significantly inhibited compared with control IgG-treated mice. ABX-MA1 treatment also suppressed experimental lung metastasis of these melanoma cells. ABX-MA1 disrupted spheroid formation by melanoma cells expressing MUC18 (homotypic interaction) and the ability of these cells to attach to human vascular endothelial cells [HUVECs (MUC18 positive)] in vitro. ABX-MA1 treatment of melanoma cells in vitro significantly inhibited the promoter and collagenase activity of matrix metalloproteinase 2, resulting in decreased invasion through Matrigel-coated filters. Decreased expression of matrix metalloproteinase 2 was also observed in the implanted tumors in vivo. Moreover, because HUVECs also express MUC18, ABX-MA1 directly disrupted the tube-like formation by HUVECs in an in vitro vessel formation assay. Collectively, these results point to usefulness of ABX-MA1 as a modality to treat melanoma either alone or in combination with conventional chemotherapy or other antitumor agents.

Animals↗

PubMed2002

Variability among Cryptosporidium parvum genotype 1 and 2 immunodominant surface glycoproteins.

Published genomic differences between Cryptosporidium parvum genotype 1 (human-derived) and genotype 2 (animal and human-derived) isolates suggest that these may belong to two distinct species. This is of significant interest since genotype 1 isolates are associated with sporadic cases of human cryptosporidiosis in 30-40 % of cases in contrast to 60-70 % of cases caused by genotype 2. The lower genetic sequence similarity between genotype 1 and 2 surface glycoproteins (gp40/15) suggests that antigenic differences should also occur, a feature that was investigated in this study. Using immune and convalescent serum samples from gnotobiotic piglets previously inoculated with genotype 1 and 2 isolates, we demonstrated that C. parvum gp15 was immunodominant for both genotype 1 and 2 isolates. Lower genetic sequence similarity between genotype 1 and 2 Cpgp40/15 did correspond to gp15 protein differences as detected by Western blot. Moreover, we confirmed that gp15 contains epitopes that are also immunodominant. Deglycosylation of C. parvum proteins resulted in decreased ability of gp15, gp23 and gp900 to react with homologous polyclonal antibodies, suggesting that these proteins also express carbohydrate epitopes. Taken together, our data suggest that there is a high phenotypic variability between C. parvum genotype 1 and 2 isolates at the level of gp15. We contemplate that gp15 surface glycoprotein plays an important role in the biology of C. parvum as a potent inducer of immune response and a possible virulence factor.

Animals↗

PubMed2002

Genetic analysis of a Cryptosporidium parvum human genotype 1 isolate passaged through different host species.

Cryptosporidium parvum TU502, a genotype 1 isolate of human origin, was passaged through three different mammalian hosts, including humans, pigs, and calves. It was confirmed to be genotype 1 by PCR-restriction fragment length polymorphism analysis of the Cryptosporidium oocyst wall protein gene, direct sequencing of PCR fragments of the small subunit rRNA and beta-tubulin genes, and microsatellite analysis. This isolate was shown to be genetically stable when passaged through the three mammalian species, with no evidence of the emergence of new subpopulations as observed by a genotype-specific PCR assay. TU502 oocysts from different sources failed to infect gamma interferon knockout mice, a characteristic of genotype 1 isolates. The genotypic and phenotypic characterization of TU502 is significant since it is the isolate selected to sequence the genome of C. parvum genotype 1 and is currently used in several research projects including human volunteer studies.

Animals↗