Biomedical subjects

Yi Sun

Publications and source records attributed to Yi Sun.

At least 37 records · Page 2Linked to original sources

PubMed2006

[Spleen-preserving distal pancreatectomy in treatment of solid-pseudopapillary neoplasm].

OBJECTIVE: To investigate the feasibility and safety of spleen-preserving distal pancreatectomy with conservation of the splenic arteries and veins in treatment of benign neoplasms of distal pancreas. METHODS: Four patients with solid-pseudopapillary neoplasm, 1 males and 3 females, aged 30 (17 - 37), underwent laparotomy. The distal pancreas with tumor was cut. The perforating branches between the splenic artery and vein and the distal pancreas were isolated, ligated, and cut. The splenic artery and vein and the short and left gastric vessels were all preserved. The spleen remained intact. RESULTS: The mean operation time was 208 minutes +/- 52 minutes, and the mean blood loss was 475 ml +/- 96 ml. Blood transfusion was not necessary. The mean post-operative hospital stay was 18 days +/- 13 days. No post-operative complications were found except for pancreatic leakage occurring in one patient that was cured by conservative treatment. No metastasis and recurrence was found. CONCLUSION: Safe and feasible, spleen-preserving distal pancreatectomy with conservation of the splenic arteries and veins is one of the best choices for treatment of benign and borderline tumors of pancreas.

Adolescent↗

PubMed2006

A phage display screen and binding studies with acetylated low density lipoprotein provide evidence for the importance of the scavenger receptor cysteine-rich (SRCR) domain in the ligand-binding function of MARCO.

MARCO is a class A scavenger receptor capable of binding both gram-negative and -positive bacteria. Using the surface plasmon resonance technique, we show here that a recombinant, soluble form of MARCO, sMARCO, binds the major gram-negative and -positive bacterial surface components, lipopolysaccharide and lipoteichoic acid. Yet, the interaction of these two polyanions with sMARCO is of much lower affinity than that of polyinosinic acid, a polyanionic inhibitor of bacterial binding to MARCO. To further elucidate the ligand-binding functions of MARCO, we performed a phage display screen with sMARCO. The screening resulted in the enrichment of only a handful of phage clones. Contrary to expectations, no polyanionic peptides, but only those with a predominantly hydrophobic nature, were enriched. One peptide, VRWGSFAAWL, was displayed on two-thirds of the phages recovered after four rounds of screening. The VRWGSFAAWL phage-sMARCO interaction had significantly slower dissociation kinetics than that between sMARCO and lipopolysaccharide or lipoteichoic acid. Further work with this phage, and the second most enriched phage, displaying the peptide RLNWAWWLSY, demonstrated that both peptides bind to the SRCR domain of MARCO, and that they probably bind to the same site. Data base searches suggested that the VRWGSFAAWL peptide represents complement component C4, but we could not convincingly confirm this suggestion. A study with chimeric scavenger receptors indicated that even minor sequence changes in the MARCO scavenger receptor cysteine-rich (SRCR) domain can have profound effects on the binding of the prototypic scavenger receptor ligand, acetylated low density lipoprotein. As shown by differential binding of glutathione S-transferase-VR-WGSFAAWL, these differences were very likely due to conformational changes. These findings led to experiments that demonstrated a crucial role of the SRCR domain for acetylated low density lipoprotein binding in MARCO. Thus, our results strengthen the notion that the SRCR domain is the major ligand-binding domain in MARCO. Furthermore, they suggest that the domain may contain multiple ligand-binding sites.

Acetylation↗

PubMed2006

Childhood injuries from motor vehicle-pedestrian collisions in Wuhan, The People's Republic of China.

OBJECTIVES: To examine motor vehicle-pedestrian collision injuries resulting in hospitalisation among children admitted into Wuhan Children's Hospital, The People's Republic of China. METHODS: From the 1993 to 2004 inpatient data of Wuhan Children's Hospital, we identified injury cases from motor vehicle traffic crashes among children aged 18 years or less using the discharge diagnosis defined by the International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM). We examined characteristics of injuries from motor vehicle traffic crashes (ICD-9-CM = E810-E819) and then calculated the proportion of injuries from motor vehicle-pedestrian collisions (ICD-9-CM = E814) among all hospitalisations for childhood injuries (ICD-9-CM = 800-959). The trend of injuries from motor vehicle-pedestrian collisions from 1993 to 2004 was described. RESULTS: Of the 12,939 injuries resulting in hospitalisation among children admitted into Wuhan Children's Hospital during 1993-2004, a total of 528 injuries were caused by motor vehicle traffic crashes. The majority of the injured children in motor vehicle traffic crashes were males (59.3%). In comparison with other traffic injuries, a higher proportion of motor vehicle-pedestrian collisions occurred among children aged 12-15 years. Motor vehicle-pedestrian collision injuries resulted in significantly longer lengths of stay in the hospital than other motor vehicle traffic injuries (19.4 days versus 14.3 days, respectively; t-test = 2.59, p-value < 0.05). The percentage of motor vehicle-pedestrian collision injuries among all hospitalisations for childhood injuries increased significantly from 1.6% (95% confidence interval [CI] = 1.2-2.1) in 1993 to 3.1% (95% CI = 2.7-3.6) in 2004 (p < 0.05). CONCLUSIONS: Hospitalisations for injuries from motor vehicle-pedestrian collisions at this large children's hospital increased significantly in the past decade. These data underscore the need for additional research and a major concerted effort to prevent motor vehicle-pedestrian collisions among children in China.

Accidents, Traffic↗

PubMed2006

Effect of aspirin plus clopidogrel on inflammatory markers in patients with non-ST-segment elevation acute coronary syndrome.

BACKGROUND: Aspirin can inhibit inflammatory reactions and platelet aggregation, but little is known about the effects of the combination of aspirin plus clopidogrel, a new antiplatelet agent, on inflammation. The purpose of this study was to determine whether aspirin plus clopidogrel can further suppress inflammation in patients with non-ST-segment elevation acute coronary syndrome (NSTEACS). METHODS: One hundred and fifteen patients with NSTEACS were randomized into two groups: group A (aspirin alone, n =58) and group B (aspirin plus clopidogrel, n =57). Patients in group A received a loading dose of 300 mg aspirin, then 100 mg per day. The patients in group B received a loading dose of 300 mg aspirin and 300 mg clopidogrel, then 100 mg aspirin and 75 mg clopidogrel per day. Serum high sensitivity C-reactive protein (hs-CRP) and tumor necrosis factor-alpha (TNF-alpha) were measured in all patients at baseline prior to any drug treatment after admission, and at 7 and 30 days after beginning drug treatment. Thirty healthy volunteers on no medications were enrolled as controls (group C). RESULTS: Baseline levels of hs-CRP and TNF-alpha in group A and group B were significantly higher than those in group C. Seven days after administration, the levels of hs-CRP in both group A and group B decreased significantly [Group A: (6.15 +/- 1.39) mg/L vs (9.18 +/- 1.62) mg/L, P <0.01; Group B:(4.99 +/- 1.62) mg/L vs (10.29 +/- 1.47) mg/L, P <0.01]. Similarly, levels of TNF- alpha in both groups decreased at 7 days compared to baseline [Group A: (90.99 +/- 28.91) pg/ml vs (117.20 +/- 37.13) pg/ml, P <0.01; Group B: (74.32 +/- 21.83) pg/ml vs (115.27 +/- 32.11) pg/ml, P <0.01]. Thirty days after administration, the levels of hs-CRP in both group A and group B decreased further to (3.49 +/- 1.53) mg/L, and (2.40 +/- 1.17) mg/L respectively (P <0.01 for both comparisons). Levels of TNF-alpha in groups A and B also decreased significantly between 7 and 30 days, to 63.28 +/- 29.01 pg/ml (group A) and (43.95 +/- 17.10) pg/ml (group B; P <0.01 for both comparisons). Significantly lower levels of hs-CRP and TNF-alpha were observed in group B compared to Group A at thirty days after initiating drug treatment (P <0.05). CONCLUSIONS: Aspirin plus clopidogrel treatment reduced levels of serum hs-CRP and TNF-alpha in patients with NSTEACS significantly more than aspirin alone. Because both aspirin and clopidogrel produce important anti-inflammatory effects, these results suggest the possibility that long-term treatment with aspirin plus clopidogrel may produce greater clinical benefits compared to treatment with aspirin alone.

Adult↗

PubMed2006

p53 and its downstream proteins as molecular targets of cancer.

The p53 tumor suppressor gene plays a key role in prevention of tumor formation through transcriptional dependent and independent mechanisms. Transcriptional-dependent mechanisms are mainly mediated by p53 regulation of downstream targets, leading to growth arrest and apoptosis. Mutational inactivation of the p53 gene is detected in more than 50% of human cancers. Mutation of p53 renders cancer cells more resistant to current cancer therapies due to lack of p53-mediated apoptosis. Extensive studies have been conducted to identify small molecules that manipulate p53, including restoration of mutant p53 conformation to wild-type, disruption of murine double minute-2 (Mdm2)-p53 binding to increase p53 level and inhibition of Mdm2 E3 ubiquitin ligase activity to prevent p53 degradation. Another approach was to identify and validate "drugable" target(s) in p53 signaling pathways that modulate p53-induced apoptosis. We profiled a p53 temperature-sensitive lung cancer cell model with the Affymetrix human HG-U133 GeneChip, covering the entire human transcriptome. We identified thousands of unique genes that were either induced or repressed in response to p53-induced apoptosis. A follow-up study characterized a p53-repressed gene, SAK, a polo-like kinase (PLK) family member, as an appealing cancer drug target. Snk/Plk-akin kinase (SAK) silencing via small interfering RNA (siRNA) induced apoptosis, whereas SAK overexpression attenuated p53-induced apoptosis. Thus, SAK repression by p53 contributes to p53-induced apoptosis. Future work is directed at determining the normal cell response to SAK silencing. If a therapeutic window is obtained, a SAK inhibitor identified from high throughput screening (HTS) could serve as a lead compound for development of a novel class of apoptosis-inducing anticancer drugs.

Humans↗

PubMed2006

Proteome analysis of combined effects of androgen and estrogen on the mouse mammary gland.

We and other investigators have previously shown that estrogen and androgen have synergistic effects on the growth of mammary epithelial ducts and alveoli in the Noble mouse. However, the molecular mechanisms behind the synergy are unknown. In the present study, we treated female FVB mice with 17-estrodial (E2) and 5-dihydrotestosterone-bezonate (DHT-B) using slow-releasing hormone pellets for 7 months. Dissection showed that hormone treatment caused atypical hyperplasia of mammary ducts and alveoli. A functional proteomic approach was used to study the holistic protein changes in mammary glands. 2-DE was used to separate proteins. Twenty-five protein spots that were differentially expressed in hormone-treated tissues compared to the control were identified by MALDI-TOF-MS, and ESI-quadrupole-TOF-MS, which include some proteins that are correlative with response to estrogen and androgen stimulation, cells differentiation and growth, signal transduction, metabolism, etc. Real-time RT-PCR was carried out to verify the different expression. These results offered some clues to understand the function of E2 and DHT-B.

Androgens↗

PubMed2006

Comparative analysis of complete mitochondrial DNA control region of four species of Strigiformes.

The sequence of the whole mitochondrial (mt) DNA control region (CR) of four species of Strigiformes was obtained. Length of the CR was 3,290 bp, 2,848 bp, 2,444 bp, and 1,771 bp for Asio flammeus, Asio otus, Athene noctua, and Strix aluco, respectively. Interestingly, the length of the control region was maximum in Asio flammeus among all the avian mtDNA control regions sequenced thus far. In addition, the base composition and organization of mtDNA CR of Asio flammeus were identical to those reported for other birds. On the basis of the differential frequencies of base substitutions, the CR may be divided two variable domains, I and III, and a central conserved domain, II. The 3' end of the CR contained many tandem repeats of varying lengths and repeat numbers. In Asio flammeus, the repeated sequences consisted of a 126 bp sequence that was repeated seven times and a 78 bp sequence that was repeated 14 times. In Asio otus, there were also two repeated sequences, namely a 127 bp sequence that was repeated eight times and a 78 bp sequence that was repeated six times. The control region of Athene noctua contained three sets of repeats: a 89 bp sequence that was repeated three times, a 77 bp sequence that was repeated four times, and a 71 bp sequence that was repeated six times. Strix aluco, however, had only one repeated sequence, a 78 bp sequence that was repeated five times. The results of this study seem to indicate that these tandem repeats may have resulted from slipped-strand mispairing during mtDNA replication. Moreover, there are many conserved motifs within the repeated units. These sequences could form stable stem-loop secondary structures, which suggests that these repeated sequences play an important role in regulating transcription and replication of the mitochondrial genome.

Animals↗

PubMed2006

Gracilarioside and gracilamides from the red alga Gracilaria asiatica.

One gracilarioside and two gracilamides with unusual cyclopropane-containing alkyl chains were isolated from the red alga Gracilaria asiatica. Their structures were determined by spectroscopic methods and microscale chemical degradation. To our knowledge, no ceramides with a cyclopropane ring have been reported from marine organisms. These three compounds were mildly cytotoxic to the human A375-S2 melanoma cell line.

Antineoplastic Agents↗

PubMed2006

Cytotoxic sterols from marine-derived fungus Pennicillium sp.

A new sterol, ergosta-8(14), 22-diene-3,5,6,7-tetraol(3beta, 5alpha, 6beta, 7alpha, 22E) (1), together with four known sterols ergosta-8(9), 22-diene-3,5,6,7-tetraol (3beta, 5alpha, 6beta, 7alpha, 22E) (2), 5alpha,8alpha-epidioxy-24(S)-methylcholesta-6,22-diene-3beta-ol (3), 5alpha,8alpha-epidioxy-24(S)-methylcholesta-6,9(11), 22-triene-3beta-ol (4), 3beta,5alpha,9alpha-trihydroxyergosta-7,22-diene-6-one (5) was isolated from marine fungus Pennicillium sp. Their structures were determined based on chemical analysis and spectral methods (IR, 1D and 2D NMR, HR-FAB-MS). Compounds 1-5 were evaluated for cytotoxicity against human liver cancer cell (Hep G), and most of them exhibited potent activity. Compound 1 display the highest potency with IC50 values 10.4 microg mL-1.

Cell Line, Tumor↗

PubMed2006

Novel mfgl2 antisense plasmid inhibits murine fgl2 expression and ameliorates murine hepatitis virus type 3-induced fulminant hepatitis in BALB/cJ mice.

Our previous reports, both experimental and human studies, have shown the importance of fibrinogen-like protein-2 (fgl2) prothrombinase in the development of fulminant viral hepatitis, a disease with a mortality of more than 80% in cases lacking immediate organ transplantation. To interfere with this potentially effective target, a 322-bp mouse fgl2 (mfgl2) antisense plasmid complementary to the exon 1 sequence of the gene, including the translation initiation site AUG, was successfully constructed. A dose-dependent inhibitory effect on mfgl2 expression by mfgl2 antisense plasmid was observed in interferon-gamma-treated RAW 264.7 cells. On hydrodynamic delivery, mfgl2 antisense plasmid significantly reduced mfgl2 expression in vivo; markedly ameliorated inflammatory cell infiltration, fibrin deposition, and hepatocyte necrosis; prolonged the survival time period; and elevated the survival rate among BALB/cJ mice with murine hepatitis virus type 3-induced fulminant hepatitis. This study may provide an effective way to interfere with the potential therapeutic target fgl2 gene for fulminant viral hepatitis and other diseases with similar pathological characteristics of microcirculation disorders, including acute rejection of xeno- or allograft transplantation and fetal loss syndrome, in which studies show fgl2 plays an important role.

Animals↗

PubMed2006

Acute myeloid leukemia-associated Mkl1 (Mrtf-a) is a key regulator of mammary gland function.

Transcription of immediate-early genes--as well as multiple genes affecting muscle function, cytoskeletal integrity, apoptosis control, and wound healing/angiogenesis--is regulated by serum response factor (Srf). Extracellular signals regulate Srf in part via a pathway involving megakaryoblastic leukemia 1 (Mkl1, also known as myocardin-related transcription factor A [Mrtf-a]), which coactivates Srf-responsive genes downstream of Rho GTPases. Here we investigate Mkl1 function using gene targeting and show the protein to be essential for the physiologic preparation of the mammary gland during pregnancy and the maintenance of lactation. Lack of Mkl1 causes premature involution and impairs expression of Srf-dependent genes in the mammary myoepithelial cells, which control milk ejection following oxytocin-induced contraction. Despite the importance of Srf in multiple transcriptional pathways and widespread Mkl1 expression, the spectrum of abnormalities associated with Mkl1 absence appears surprisingly restricted.

Animals↗

PubMed2006

E3 ubiquitin ligases as cancer targets and biomarkers.

E3 ubiquitin ligases are a large family of proteins that are engaged in the regulation of the turnover and activity of many target proteins. Together with ubiquitin-activating enzyme E1 and ubiquitin-conjugating enzyme E2, E3 ubiquitin ligases catalyze the ubiquitination of a variety of biologically significant protein substrates for targeted degradation through the 26S proteasome, as well as for nonproteolytic regulation of their functions or subcellular localizations. E3 ubiquitin ligases, therefore, play an essential role in the regulation of many biologic processes. Increasing amounts of evidence strongly suggest that the abnormal regulation of some E3 ligases is involved in cancer development. Furthermore, some E3 ubiquitin ligases are frequently overexpressed in human cancers, which correlates well with increased chemoresistance and poor clinic prognosis. In this review, E3 ubiquitin ligases (such as murine double minute 2, inhibitor of apoptosis protein, and Skp1-Cullin-F-box protein) will be evaluated as potential cancer drug targets and prognostic biomarkers. Extensive study in this field would lead to a better understanding of the molecular mechanism by which E3 ligases regulate cellular processes and of how their deregulations contribute to carcinogenesis. This would eventually lead to the development of a novel class of anticancer drugs targeting specific E3 ubiquitin ligases, as well as the development of sensitive biomarkers for cancer treatment, diagnosis, and prognosis.

Animals↗

PubMed2006

SAG/ROC-SCF beta-TrCP E3 ubiquitin ligase promotes pro-caspase-3 degradation as a mechanism of apoptosis protection.

Skp1-cullin-F-box protein (SCF) is a multicomponent E3 ubiquitin (Ub) ligase that ubiquitinates a number of important biologic molecules such as p27, beta-catenin, and IkappaB for proteasomal degradation, thus regulating cell proliferation and survival. One SCF component, SAG/ROC2/Rbx2/Hrt2, a RING finger protein, was first identified as a redox-inducible protein, which, when overexpressed, inhibited apoptosis both in vitro and in vivo. We report here that sensitive to apoptosis gene (SAG), as well as its family member ROC1/Rbx1, bound to the proinactive form of caspase-3 (pro-caspase-3). Binding was likely mediated through F-box protein, beta-transducin repeat-containing protein (beta-TrCP), which binds to the first 38 amino acids of pro-caspase-3. Importantly, beta-TrCP1 expression significantly shortened the protein half-life of pro-caspase-3, whereas expression of a dominant-negative beta-TrCP1 mutant with the F-box domain deleted extended it. An in vitro ubiquitination assay showed that SAG/ROC-SCF(beta-TrCP) promoted ubiquitination of pro-caspase-3. Furthermore, endogenous levels of pro-caspase-3 were decreased by overexpression of SAG/ROC-SCF(beta-TrCP) E3 Ub ligases, but increased on siRNA silencing of SAG, regulator of cullin-1 (ROC1), or beta-TrCPs, leading to increased apoptosis by etoposide and TNF-related apoptosis-inducing ligand through increased activation of caspase-3. Thus, pro-caspase-3 appears to be a substrate of SAG/ROC-SCF(beta-TrCP) E3 Ub ligase, which protects cells from apoptosis through increased apoptosis threshold by reducing the basal level of pro-caspase-3.

Apoptosis↗

PubMed2006

[Effect of perioperative continuous epidural morphine administration on plasma D-dimer in patients undergoing total hip replacement].

OBJECTIVE: To evaluate the effect of perioperative continuous epidural morphine administration on plasma D-dimer level in patients undergoing total hip replacement. METHODS: Forty ASA I-II patients undergoing total hip replacement under epidural anesthesia were randomized into two groups. In one group, the patients were given epidural administration of morphine 15 min before operation at 4 mg (in 10 ml normal saline) and for 48 h after the operation at 80 microg/h, while those in the other group received epidural injection of the same amount of normal saline before operation and 0.15% ropivacaine 2.0 ml/h for 48 h in the same manner after operation. Blood samples were taken before anesthesia (T(0)), at the end of operation (T(1)), and 24 h and 48 h after operation (T(2) and T(3)) for determination of plasma IL-6 and D-dimer levels. RESULTS: In both groups plasma IL-6 and D-dimer levels showed significant increase at T(1), T(2) and T(3) in comparison with those at T(0), and their levels were significantly lower in morphine group than in ropivacaine group at T(1), T(2) and T(3). CONCLUSION: Epidural morphine can lower plasma IL-6 and D-dimer levels and correct blood hypercoagulability in patients undergoing total hip replacement.

Aged↗

PubMed2006

[Peri-uvulopalatopharyngoplasty electroencephalogram spectral power analysis in patients with obstructive sleep apnea-hypopnea syndrome].

OBJECTIVE: To study the peri-uvulopalatopharyngoplasty (UPPP) effects on EEG spectral power changes in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS). METHOD: Fifty-four cases were included. The diagnosis was made by polysomnography (PSG). C3/A2 was analyzed by using fast Fourier transform (FFT). Spectral edge frequency (SEF), median power frequency (MPF). a-index, beta-index, delta-index and theta-index were compared with those peri-UPPP treatment. RESULT: Sleep architecture was improved after UPPP. The ratio of slow wave sleep increased. A decrease of mean SEF in total sleep period. The mean MPF was decreased during stage IV. a-index and beta-index were decreased, delta-index and theta-index were increased after the therapy. CONCLUSION: The UPPP therapy has an acute effect in improving the sleep architecture and EEG power spectrum. These changes may be related to the recovery of cerebral function in patients with OSAHS.

Adult↗

PubMed2006

A new cyclotetrapeptide from marine fungus Trichoderma reesei.

A new cyclotetrapeptide, trichoderide A, was isolated from the marine fungus Trichoderma reesei. The structure was identified by spectral methods, and the stereochemical assignments were made by chiral HPLC of the hydrolyzed compound. Trichoderide A showed moderate cytotoxity against human A375-S2 melanoma cell line.

Amino Acids↗

PubMed2006

Improving computational predictions of cis-regulatory binding sites.

The location of cis-regulatory binding sites determine the connectivity of genetic regulatory networks and therefore constitute a natural focal point for research into the many biological systems controlled by such regulatory networks. Accurate computational prediction of these binding sites would facilitate research into a multitude of key areas, including embryonic development, evolution, pharmacogenemics, cancer and many other transcriptional diseases, and is likely to be an important precursor for the reverse engineering of genome wide, genetic regulatory networks. Many algorithmic strategies have been developed for the computational prediction of cis-regulatory binding sites but currently all approaches are prone to high rates of false positive predictions, and many are highly dependent on additional information, limiting their usefulness as research tools. In this paper we present an approach for improving the accuracy of a selection of established prediction algorithms. Firstly, it is shown that species specific optimization of algorithmic parameters can, in some cases, significantly improve the accuracy of algorithmic predictions. Secondly, it is demonstrated that the use of non-linear classification algorithms to integrate predictions from multiple sources can result in more accurate predictions. Finally, it is shown that further improvements in prediction accuracy can be gained with the use of biologically inspired post-processing of predictions.

Algorithms↗

PubMed2006

[Expressions of TGF-betaR I, Smad2, Smad3 and Smad7 in keloids].

OBJECTIVE: To investigate the expression of TGF-betaR I, Smad2, Smad3 and Smad7 in keloids, normal scars and normal skins. Discuss the significance of these proteins in the course of keloid. METHODS: Immunohistochemistry method was used to detect the expression intensity and distribution of these proteins in above 3 kinds of different tissues in 44 cases. Statistics was used to analyze the data. RESULTS: The expression of TGF-betaR I were much stronger in keloid than in the other two tissues. The expression of Smad7 were lower in keloids. The increase expression of Smad2,3 were not obvious, but they were found to accumulate in the nucleus. CONCLUSIONS: The results indicate that over-expression of TGF-betaR I, low-expression of Smad7 and accumulation of Smad2,3 may be one of the etiological factors of keloids. This research may provide a new idea to prevent and treat keloids or other fibrosis diseases in the future.

Adolescent↗