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Tao Su

Publications and source records attributed to Tao Su.

14 recordsLinked to original sources
PubMed2026

Quantitative N-glycoproteomic analysis reveals glycosylation signatures of plasma immunoglobulin G in sepsis.

INTRODUCTION: Sepsis is a life-threatening condition resulting from organ dysfunction due to a dysregulated immune response to infection. Immunoglobulin G (IgG) plays a role in modulating immune responses. However, the precise IgG subclass-specific N-glycosylation profiles in patients with sepsis remain poorly characterized. METHODS: This study aimed to define the site-specific N-glycosylation signatures of plasma IgG subclasses in sepsis patients with different prognoses using quantitative glycoproteomics. By employing our established GlycoQuant strategy, we quantified the intact N-glycopeptides (IGPs) of IgG subclasses in 40 healthy controls and 40 sepsis patients with a clear prognosis. RESULTS: We identified 12 IGPs with altered abundances between patients with sepsis and healthy controls. After Benjamini-Hochberg (BH) correction of the 31 outcome-stratified IGP comparisons, IGP24 and IGP25 remained significant and met the prespecified fold-change criterion. Global BH correction across 124 IGP-clinical parameter correlations retained positive associations of IGP19, IGP22, and IGP23 with procalcitonin (PCT). In exploratory outcome-stratified ROC analyses, candidates were selected using the original unadjusted P-value and fold-change screen; five IGPs were evaluated, with IGP25 and IGP24 yielding the highest individual AUCs. Collectively, our findings underscore the potential of IgG subclass-specific glycosylation profiling as a novel translational approach for clinical applications in sepsis management. SIGNIFICANCE: Sepsis remains a leading cause of global mortality, with patient outcomes heavily dependent on timely diagnosis and accurate prognosis. The dysregulated host immune response, particularly involving immunoglobulins, is central to its pathophysiology. This study provides a significant advance in the field of clinical glycoproteomics by applying a quantitative, site-specific strategy to delineate the plasma IgG subclass N-glycosylation landscape in sepsis. We report, for the first time, a panel of subclass-specific intact IgG N-glycopeptides (IGPs) that are significantly altered in sepsis patients compared to healthy controls. The identified IGPs not only demonstrate diagnostic and prognostic potential but also show a significant correlation with procalcitonin, a key clinical severity index. These findings bridge a critical knowledge gap by moving beyond bulk IgG glycosylation analysis to subclass-resolved profiling, offering novel molecular insights into sepsis immunopathology. The identified glycosylation signatures hold substantial translational promise as a foundation for developing innovative, glycan-based biomarker panels to improve the precision management of this heterogeneous and life-threatening syndrome.

Humans↗
PubMed2005

Experimental and theoretical investigation of single Cu, Ag, and Au atoms adsorbed on Si(111)-(7x7).

Using scanning tunneling microscopy and first principles calculations, the adsorption sites of single Cu, Ag, and Au atoms on the Si(111)-(7x7) surface have been systematically investigated and identified. Despite their monovalence, these atoms were found to adsorb at high coordination sites, seeking to saturate the maximum number of dangling bonds. The stable adsorption sites were further observed to be distinctly different in the faulted and unfaulted half unit cells, showing an asymmetry that has never been observed for many other adsorbates.

Journal Article↗
PubMed2005

Headspace water-based liquid-phase microextraction.

A new organic-free mode of headspace liquid-phase microextraction termed headspace water-based liquid-phase microextraction has been developed. Five phenols were used as model compounds in the development and evaluation of the procedure. Parameters affecting the extraction efficiency were investigated. Under optimal extraction conditions, very high enrichment factors were achieved. Since only water (with sodium hydroxide to adjust the pH) and a conventional microsyringe were used, this new technique is affordable, efficient, and convenient for extraction of volatile and semivolatile ionizable compounds. In addition, in combination with capillary electrophoresis, the entire analytical process is totally organic solvent-free and is thus environmentally friendly.

Chemistry Techniques, Analytical↗
PubMed2005

PIK3CA mutations correlate with hormone receptors, node metastasis, and ERBB2, and are mutually exclusive with PTEN loss in human breast carcinoma.

Deregulation of the phosphatidylinositol 3-kinase (PI3K) pathway either through loss of PTEN or mutation of the catalytic subunit alpha of PI3K (PIK3CA) occurs frequently in human cancer. We identified PIK3CA mutations in 26% of 342 human breast tumor samples and cell lines at about equal frequency in tumor stages I to IV. To investigate the relationship between PTEN and PIK3CA, we generated a cohort of tumors that had lost PTEN expression and compared it with a matched control set that had retained PTEN. A highly significant association between PIK3CA mutations and retention of PTEN protein expression was observed. In addition, PIK3CA mutations were associated with expression of estrogen and progesterone receptors (ER/PR), lymph node metastasis, and ERBB2 overexpression. The fact that PIK3CA mutations and PTEN loss are nearly mutually exclusive implies that deregulated phosphatidylinositol-3,4,5-triphosphate (PIP(3)) is critical for tumorigenesis in a significant fraction of breast cancers and that loss of PIP(3) homeostasis by abrogation of either PIK3CA or PTEN relieves selective pressure for targeting of the other gene. The correlation of PIK3CA mutation to ER/PR-positive tumors and PTEN loss to ER/PR-negative tumors argues for disparate branches of tumor evolution. Furthermore, the association between ERBB2 overexpression and PIK3CA mutation implies that more than one input activating the PI3K/AKT pathway may be required to overcome intact PTEN. Thus, mutation of PIK3CA is frequent, occurs early in carcinoma development, and has prognostic and therapeutic implications.

Adult↗
PubMed2005

Study of antiepileptic effect of extracts from Acorus tatarinowii Schott.

PURPOSE: To study the antiepileptic properties of extracts from rhizomes of Acorus tatarinowii Schott (ATS). METHODS: The decoction and volatile oil were extracted from rhizomes of ATS by traditional decocting and supercritical CO(2) fluid extraction (SFE-CO(2)) methods. Maximal electroshock (MES), pentylenetetrazol (PTZ) maximal seizure, and prolonged PTZ kindling models were used to test their anticonvulsive properties. The gamma-aminobutyric acid (GABA) immunohistochemical reaction (IR) was used to study GABAergic neuron changes in the PTZ kindling model and the effects of treatment. RESULTS: Both decoction (dose; 10-20 g/kg) and volatile oil (1.25 g/kg) of ATS decreased the convulsive rate significantly in the MES model. Decoction of ATS was shown to be effective in the PTZ model with both decreased convulsive and mortality rates. The volatile oil of ATS failed to prevent seizures in the dose range tested, although prolonged seizure latency and decreased mortality were found at a dose of 1.25 g/kg. In the PTZ kindling model, GABA-IR neurons decreased obviously compared with the normal group. In the groups treated with the decoction and volatile oil, the seizure intensity decreased significantly after treatment. Increased GABA-IR neurons also were found when compared with PTZ kindling controls. Morphologic observation also showed that GABA-IR neuron damage was less severe in the drug-treated groups. CONCLUSIONS: Both decoction and volatile oil extracted from the rhizome of Acorus tatarinowii Schott have anticonvulsive effects. The volatile oil is shown to be less effective for PTZ-induced convulsions. Both extracts can prevent convulsions as well as convulsion-related GABAergic neuron damage in the brain in the prolonged PTZ kindling model.

Acorus↗
PubMed2005

[Chloroplast genetic engineering: a new approach in plant biotechnology].

Chloroplast genetic engineering, offers several advantages over nuclear transformation, including high level of gene expression, increased biosafety, remedying some limitations associated with nuclear genetic transformation, such as gene silencing and the stability of transformed genes. It is now regarded as an attractive new transgenic technique and further development of biotechnology in agriculture. In this article we reviewed the characteristics, applications of chloroplast genetic engineering and its promising prospects were discussed.

Biotechnology↗
PubMed2004

Adenoviral mediated transfer of TIMP-3 partially prevents glutamate-induced cell death in primary cultured cortical neurons of the rat.

Metalloproteinases and tissue inhibitor of metalloproteinases (TIMPs) are associated with tissue reorganization after injury. The up-regulation of TIMP-3 has recently been found in ischemic brain although its functional implications are unclear. In this study we show that overexpression of TIMP-3 by adenovirus-mediated gene transfer partially protects neurons against excitotoxic death induced by glutamate in culture. The partial neuroprotection afforded by TIMP-3 has implications for our understanding of the physiological role of TIMP-3 in the normal and damaged central nervous system.

Adenoviridae↗
PubMed2004

Role of mPKCI, a novel mu-opioid receptor interactive protein, in receptor desensitization, phosphorylation, and morphine-induced analgesia.

The human mu-opioid receptor (HmuOR) is a G-protein coupled receptor that mediates analgesia, euphoria and other important central and peripheral neurological functions. In this study, we found in a yeast two-hybrid screen that a protein kinase C-interacting protein (PKCI) specifically interacts with the C terminus of HmuOR. The interaction of PKCI with HmuOR was recapitulated in Chinese hamster ovary cells that express the full-length HmuOR and PKCI proteins. The affinity of HmuOR for an opioid ligand and its ability to mediate the activation of a G-protein were not altered by their interaction. However, the association of PKCI with HmuOR reduced agonist-induced inhibition of adenylyl cyclase and suppressed HmuOR desensitization partially at the G protein level and completely at the adenylyl cyclase level. Furthermore, PMA-induced, but not DAMGO-induced, HmuOR phosphorylation was partially inhibited by the coexpression of PKCI, suggesting that PKCI exerts a selective regulatory effect on HmuOR signaling. This effect was specific to the mu-opioid receptor because delta-opioid receptor desensitization was unaffected by PKCI. In addition, behavioral studies revealed that both basal and morphine-induced analgesia were significantly enhanced in the mutant mice that lacked expression of PKCI gene, and these mice developed a greater extent of tolerance to morphine analgesia. Taken together, these results suggest that PKCI functions as a negative regulator in HmuOR desensitization, phosphorylation, and in mediating morphine analgesia.

Amino Acid Sequence↗
PubMed2004

[Studies on pharmacodynamic characteristics of aristolochic acid I in rats].

OBJECTIVE: To study pharmacodynamic characteristics by oral administration aristolochic acid I (AA-I) in rats. METHOD: After one-time oral administration of Aristolochiae manshuriensis decoction 10 g x kg(-1) and 125I labeled AA-I (containing AA-I 37.2 microg x mL(-1)), whole blood concentration of 125I-AA-I and the binding rate of serum albumin were detected in 69 normal wistar male rats. Metabolic dynamic parameters were calculated by program 3P87 with a two compartment model. The distribution ratio and ID% of nine viscera or tissue were measured and compared with other until the 40th day. RESULT: After oral administration, AA-I was rapidly absorbed into the blood and reached its peak at 30 minutes and lasted till 90 minutes. AA-I concentration in the blood gradually declined afterwards. 24 hours later, only few AA-I could be detected. By the 10th day, 68.5% of AA-I presented as the binding type with serum albumin. Pharmacodynamic parameters were calculated as follows: Tmax 0.74 h, Cmax 0.92 microg x mL(-1), t1/2alpha 0.68 h, t1/2beta 20.46 h, V/F 87.39 mL, CL(s) 5.85 mL x h(-1) (0.10 mL x min(-1)). On the other hand, after oral administration AA-I was rapidly distributed to all the viscera or tissue, whose peak appeared in 5 minutes and the vallecula was from 24 to 48 hours. The distribution ratio of AA-I rose in the kidney after 24 hours, and it showed the highest level in the kidney and in the liver by the 4th day compared with other organs or tissue (P < 0.05). However, the distribution ratio of AA-I in the kidney became the most dominant one after the 30th and the 40th day compared with the others (P < 0.05). CONCLUSION: AA-I is rapidly absorbed after oral administration in rats. Its distribution has the organ specificity, which is characterized as the possible partial metabolism in the liver and the accumulation in the kidney because of rather slower elimination. The characteristics may be related to the long term nephrotoxicity of AA-I.

Administration, Oral↗
PubMed2003

Deletion of histidine triad nucleotide-binding protein 1/PKC-interacting protein in mice enhances cell growth and carcinogenesis.

PKC-interacting protein (PKCI), also designated histidine triad nucleotide-binding protein 1, belongs to the histidine triad (HIT) family of proteins. Its structure is highly conserved from bacteria to humans and shares homology with the tumor-suppressor gene fragile histidine triad (FHIT). Although it was originally thought to inhibit PKC, its actual physiologic function is not known. Therefore, we used the technique of homologous recombination to generate homozygous deleted PKCI-/- mice. These mice display normal fetal and adult development. However, when mouse embryo fibroblasts were established from 13.5-day embryos and serially passaged the PKCI-/- cells displayed an increase in growth rate and underwent spontaneous immortalization, whereas the PKCI+/+ cells senesced and ceased growing. Furthermore, the PKCI-/- mouse embryo fibroblasts displayed increased resistance to cytotoxicity by ionizing radiation. In view of these findings we examined possible effects of PKCI on susceptibility to carcinogenicity. Both PKCI+/+ and PKCI-/- mice were treated with the chemical carcinogen N-nitrosomethylbenzylamine (NMBA) by intragastric administration and killed 12 weeks later. As expected with this protocol, NMBA induced squamous tumors (both papillomas and carcinomas) of the forestomach. The incidence, multiplicity per mouse, volume, and degree of malignancy of these tumors were significantly greater in the PKCI-/- than in the PKCI+/+ mice. Furthermore, four adenomas and one adenocarcinoma of the glandular stomach were found in the NMBA-treated PKCI-/- mice but no tumors of the glandular stomach were found in the NMBA-treated PKCI+/+ mice or in any of the untreated mice. Taken together, these findings suggest that, like FHIT, PKCI may normally play a tumor-suppressor role. The possible role of PKCI as a tumor suppressor in humans remains to be determined.

Animals↗
PubMed2003

Polarized epithelial membrane traffic: conservation and plasticity.

Most cells are polarized and have distinct plasma membrane domains, which are the result of polarized trafficking of proteins and lipids. Great progress has been made in elucidating the highly conserved polarized targeting machinery. A pre-eminent challenge now is to understand the plasticity of polarized traffic, how it is altered by differentiation and dedifferentiation during development, as well as the adaptation of differentiated cells to meet changing physiological needs.

Animals↗
PubMed2003

Length of Epstein-Barr virus termini as a determinant of epithelial cell clonal emergence.

Reiterated terminal sequences of Epstein-Barr virus (EBV) DNA are numerically heterogeneous among infectious virions, providing a viral measure of clonality in infected cells. After in vitro infection, carcinoma cells bearing EBV episomes with fewer terminal repeats (TRs) proliferated faster. In single-cell clones, TR number varied inversely to the quantity of latent membrane protein 2A (LMP2A) transcripts whose unspliced precursors cross joined TRs. Thus, EBV clonality may reflect selection for a TR number that optimizes LMP2A-enhanced tumor progression, with infection occurring after epithelial cell transformation.

Cell Transformation, Viral↗
PubMed2002

A defective, rearranged Epstein-Barr virus genome in EBER-negative and EBER-positive Hodgkin's disease.

A ubiquitous herpesvirus that establishes life-long infection, the Epstein-Barr virus (EBV) has yielded little insight into how a single agent in general accord with its host can produce diverse pathologies ranging from oral hairy leukoplakia to nasopharyngeal carcinoma, from infectious mononucleosis to Hodgkin's disease (HD) and Burkitt's lymphoma. Its pathogenesis is further confounded by the less than total association of virus with histologically similar tumors. In other viral systems, defective (interfering) viral genomes are known to modulate outcome of infection, with either ameliorating or intensifying effects on disease processes initiated by prototype strains. To ascertain whether defective EBV genomes are present in HD, we examined paraffin-embedded tissue from 56 HD cases whose EBV status was first determined by cytohybridization for nonpolyadenylated EBV RNAs (EBERs). Using both standard polymerase chain reaction (PCR) and PCR in situ hybridization, we successfully amplified sequences that span abnormally juxtaposed BamHI W and Z fragments characteristic of defective heterogeneous (het) EBV DNA from 10 of 32 (31%) EBER-positive tumors. Of 24 EBER-negative HD, 8 yielded PCR products indicating presence of het EBV DNA. Two of these contained defective EBV in the apparent absence of the prototype virus. Of the 42 tumors analyzed for defective EBV by both PCR techniques, there was concordance of results in 38 (90%). Detection of defective EBV genomes with the potential to disrupt viral gene regulation suggests one mechanism for pathogenic diversity that may also account for loss of prototypic EBV from individual tumor cells.

Adult↗