PubMed Health⌕ Search

Biomedical subjects

Y Shan

Publications and source records attributed to Y Shan.

At least 19 recordsLinked to original sources

The clinical value of serum CEA, CA19-9, and CA242 in the diagnosis and prognosis of pancreatic cancer.

AIM: Serum tumour markers carcinoembryonic antigen (CEA), carbohydrate antigen 19-9 (CA19-9) and CA242 were investigated to evaluate the values of single and combined test in the diagnosis and prognosis of pancreatic cancer. METHODS: Pre-operative serum CEA, CA19-9 and CA242 were measured in 105 pancreatic cancers, 70 non-pancreatic malignancies and 30 benign pancreatic diseases. RESULTS: The sensitivity of CA19-9 alone was the highest in pancreatic cancer patients (80%), but the specificity was significantly lower than that of CEA and CA242 (P<0.01). The combination of CEA and CA242 could increase the specificity to 92%. In serum CA242 positive patients, the survival time was remarkably shorter than that of patients with negative result (P<0.01). The survival time in patients with more than two markers positive expression of CEA, CA19-9 and CA242 was obviously shorter than that of only one or no marker positive expression (P<0.05). CONCLUSION: The diagnostic rate of CA19-9 in pancreatic cancer is better than that of CEA and CA242. Combined detection of CEA and CA242 can improve the diagnostic specificity obviously. High levels of serum markers are associated with advanced stage of the disease. Patients with two or three markers positive expression of CEA, CA19-9, and CA242 simultaneously had a shorter survival time.

Adult↗

Cloning and characterization of the mouse Arht2 gene which encodes a putative atypical GTPase.

ARHT is a new subgroup of the Rho family identified recently, which consists of two Rho-like genes, Arht1 and Arht2. ARHT may be involved in mitochondrial homeostasis and apoptosis. Constitutively active mutants of ARHT1 induced an aggregation of the mitochondrial network and resulted in an increased apoptotic rate of the cells. Here we report the molecular cloning and characterization of a novel mouse cDNA encoding a putative atypical GTPase protein, Arht2. Mouse Arht2 consists of 19 exons and has been mapped to mouse chromosome 17A3.3. Both human and mouse Arht2 genes are ubiquitously expressed in adult tissues. The results of RT-PCR experiments indicated that the Arht2 gene is expressed in all stages of mouse testis and reached the adult level of transcription at postnatal day 30. In situ hybridization revealed strong hybridization signals of Arht2 in residual bodies. In the mouse testis, Arht2 may be involved in the differentiation of testis and spermiogenesis. The molecular characterization of the mouse Arht2 gene may provide a clue for functional studies of the human ARHT genes.

Amino Acid Sequence↗

Prediction of protein interaction sites from sequence profile and residue neighbor list.

Protein-protein interaction sites are predicted from a neural network with sequence profiles of neighboring residues and solvent exposure as input. The network was trained on 615 pairs of nonhomologous complex-forming proteins. Tested on a different set of 129 pairs of nonhomologous complex-forming proteins, 70% of the 11,004 predicted interface residues are actually located in the interfaces. These 7732 correctly predicted residues account for 65% of the 11,805 residues making up the 129 interfaces. The main strength of the network predictor lies in the fact that neighbor lists and solvent exposure are relatively insensitive to structural changes accompanying complex formation. As such, it performs equally well with bound or unbound structures of the proteins. For a set of 35 test proteins, when the input was calculated from the bound and unbound structures, the correct fractions of the predicted interface residues were 69 and 70%, respectively.

Computational Biology↗

Fold recognition and accurate query-template alignment by a combination of PSI-BLAST and threading.

A homology-based structure prediction method ideally gives both a correct fold assignment and an accurate query-template alignment. In this article we show that the combination of two existing methods, PSI-BLAST and threading, leads to significant enhancement in the success rate of fold recognition. The combined approach, termed COBLATH, also yields much higher alignment accuracy than found in previous studies. It consists of two-way searches both by PSI-BLAST and by threading. In the PSI-BLAST portion, a query is used to search for hits in a library of potential templates and, conversely, each potential template is used to search for hits in a library of queries. In the threading portion, the scoring function is the sum of a sequence profile and a 6x6 substitution matrix between predicted query and known template secondary structure and solvent exposure. "Two-way" in threading means that the query's sequence profile is used to match the sequences of all potential templates and the sequence profiles of all potential templates are used to match the query's sequence. When tested on a set of 533 nonhomologous proteins, COBLATH was able to assign folds for 390 (73%). Among these 390 queries, 265 (68%) had root-mean-square deviations (RMSDs) of less than 8 A between predicted and actual structures. Such high success rate and accuracy make COBLATH an ideal tool for structural genomics.

Algorithms↗

Identification of an 85-kb DNA fragment containing pms1, a locus for photoperiod-sensitive genic male sterility in rice.

Photoperiod-sensitive genic male-sterile rice has a number of desirable characteristics for hybrid rice production. Previous studies identified pms1, located on chromosome 7, as a major locus for photoperiod-sensitive genic male sterility. The objective of this study was to localize the pms1 locus to a specific DNA fragment by genetic and physical mapping. Using 240 highly sterile individuals and a random sample of 599 individuals from an F2 population of over 5000 individuals from a cross between Minghui 63 and 32001S, we localized the pms1 locus by molecular marker analysis to a genetic interval of about 4 cM, 0.25 cM from RG477 on one side and 3.8 cM from R1807 on the other side. A contig map composed of seven BAC clones spanning approximate 500 kb in length was constructed for the pms1 region by screening a BAC library of Minghui 63 DNA using RFLP markers and chromosomal walking. Analysis of recombination events in the pms1 region among the highly sterile individuals reduced the length of the contig map to three BAC clones. Sequencing of one BAC clone, 2109, identified two SSR markers located 85 kb apart in the clone that flanked the pms1 locus on both sides, as indicated by the distribution of recombination events. We thus concluded that the pms1 locus was located on the fragment bounded by the two SSR markers.

Chromosome Mapping↗

Natural course of schizophrenia: 2-year follow-up study in a rural Chinese community.

BACKGROUND: A number of studies have questioned whether the natural course of schizophrenia is more favourable in "developing" than "developed" societies and whether culture is a factor in producing a favourable course. AIMS: This prospective study tests the hypothesis that the natural outcome of schizophrenia would be favourable in a Chinese rural area. METHOD: We investigated all patients with schizophrenia, including patients who had not received any treatment, among 149 231 rural community population in Xinjin County, Sichuan in 1994. Those patients who had never received treatment were followed up for two years. RESULTS: Three-quarters of patients with schizophrenia who had not been treated remained symptomatic. As the duration of illness increased, the illness became more serious. The clinical outcome of the drug-treatment group was significantly better than for patients who had not received any treatment. CONCLUSIONS: The natural clinical outcome of schizophrenia in the Chinese rural community was poor, and occupational functioning of patients with schizophrenia was comparatively better. Schizophrenia itself has a specific natural course--antipsychotic drug treatment and psychosocial treatment will produce an improvement in prognosis.

Adolescent↗

The regulatory effect of ERK1/2 signal pathway on production of TNFalpha induced by LPS in mice Kupffer cells.

OBJECTIVE: To study the rule of ERK1/2 activity and regulative effect of ERK1/2 pathway on the production of pro-inflammatory cytokine TNFalpha in mice Kupffer cells (mKC) induced by LPS, and to exploring novel methods to prevent and treat clinical patients of endotoxemia. METHODS: Immunoprecipitate kinase assay and Western blotting analysis were used to detect the phosphorylated ERK1/2 kinase activity in mKC stimulated by LPS, and ELISA was used to study the effect of ERK1/2 signaling cascade on LPS-induced TNFalpha production in mKC. RESULTS: In mKC, LPS treatment resulted in transient and rapid increase of kinase activity of ERK1/2 that phosphorylated their specific substrate ELK-1, with maximal value at 30 minutes and a return near to baseline within 2 hours, and LPS-induced ERK1/2 activity from LPS concentration of 10 pg/ml to the top activity at 100 ng/ml. No activity was observed in unstimulated mKC. Inhibition of the ERK1/2 pathway using the specific ERK1/2 signal pathway inhibitor PD98059 caused a marked and concentration-dependent reduction of TNFalpha production. CONCLUSIONS: The results show that LPS can markedly activate ERK1/2 pathway in mKC. PD98059 causes a significant and concentration-dependent reduction of TNFalpha production. ERK1/2 may be a novel target to treat clinical patient of endotoxemia.

Animals↗

[The impact of lateral rhinotomy on nasal airway].

OBJECTIVE: In order to ascertain the lateral operation and medial maxillectomy affect on nasal airway. METHOD: Report 16 cases of nasal cavity or nasal sinus neoplasm who were therapied by lateral rhinotomy and medial maxillectomy. They were observed by acoustic rhinometer (AR) and CT examination in 1-2.5 years after the surgery. RESULT: The feeling of nasal obstruct were disappeared in 3 months after the surgery. The nasal airway resistance(NAR) of the ill nasal cavity was markedly decreased after the surgery, and the total NAR were decreasing unmarkably. The mucous proliferation was notable only in the first year after surgery, and especially on remains of the inferior turbinate or extra wall of nasal cavity. CONCLUSION: Lateral rhinotomy operation and medial maxillectomy have less impact on nasal airway and the functions.

Adult↗

Induction of the heme oxygenase-1 gene by metalloporphyrins.

Induction of expression of heme oxygenase-1 (HO-1) has been studied in primary cultures of chick embryo liver cells and in the LMH line of avian hepatoma cells. Cells were transiently transfected with selected constructs containing portions of the 5'-untranslated (promoter) region of the HO-1 gene linked to luciferase as reporter gene. LMH cells that had been stably transfected with selected wild type or mutant constructs were also studied. Metalloporphyrins, especially Fe protoporphyrin (heme) and Co protoporphyrin strongly induced luciferase expression in both types of transfected cells. Low concentrations of Zn mesoporphyrin, an inhibitor of HO activity, exerted a synergistic effect on heme-, but not Co protoporphyrin-dependent induction. The antioxidant and &bond;SH donor N-acetyl cysteine had little effect on the metalloporphyrin-dependent inductions of HO-1, in contrast to its marked inhibitory effect on the sodium arsenite-dependent induction of the HO-1 gene. Deletional analysis showed that the key element(s) required for the metalloporphyrin-dependent induction of HO-1 is located between -3.6 and -5.6 kb upstream of the transcription starting point. Data from electrophoretic mobility shift and site-directed mutagenesis experiments excluded a role for consensus AP-1 binding elements at -1576, -3647, or -4578 in the inductions produced by heme or Co protoporphyrin.

Animals↗

Upstream regulatory elements in chick heme oxygenase-1 promoter: a study in primary cultures of chick embryo liver cells.

Previously, chick heme oxygenase-1 (cHO-1) gene was cloned by us and two regions important for induction by sodium arsenite were identified. These two regions were found to contain consensus sequences of an AP-1 (-1580 to -1573) and a MRE/cMyc complex (-52 to -41). In the current study, the roles of these two elements in mediating the sodium arsenite or cobalt chloride dependent induction of cHO-1 were investigated further. DNA binding studies and site-directed mutagenesis studies indicated that both the AP-1 and MRE/cMyc elements are important for the sodium arsenite induction, while cobalt chloride induction involves only the AP-1 element. Electrophoretic mobility shift assays showed that nuclear protein binding to the AP-1 element was increased by both sodium arsenite or cobalt chloride treatment, whereas the binding of proteins to the MRE/cMyc element showed a high basal expression in untreated cells and the binding activity was only slightly increased by sodium arsenite treatment. Site-directed mutagenesis studies showed that, to completely abolish sodium arsenite induction, both the AP-1 and MRE/cMyc elements must be mutated; mutation of either element alone resulted in only a partial effect. In contrast, a single mutation at AP-1 element was sufficient to reduce the cobalt chloride induction almost completely. The MRE/cMyc complex plays a major role in the basal level expression, and shares some similarities to the upstream stimulatory factor element (USF) identified in the promoter regions of mammalian HO-1 genes and other stress regulated genes. Because sodium arsenite is known to cause oxidative stress and because activation of AP-1 proteins has been shown to be a key step in the oxidative stress response pathway, we also explored the possibility that the induction of the cHO-1 gene by sodium arsenite is mediated through oxidative stress pathway(s) by activation of AP-1 proteins. We found that pretreatment with antioxidants (N-acetyl cysteine or quercetin) reduced the induction of the endogenous cHO-1 message or cHO-1 reporter construct activities induced by sodium arsenite or cobalt chloride. These antioxidants also reduced the protein binding activities to the AP-1 element in the electrophoretic mobility shift assays. In summary, induction of the cHO-1 gene by sodium arsenite or cobalt chloride is mediated by activation of the AP-1 element located at -1,573 to -1,580 of the 5'UTR.

Animals↗

CADASIL: the dermatologic diagnosis of a neurologic disease. Cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy.

Cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is an increasingly recognized neurologic disease characterized by pathognomonic changes to the small vessels, particularly in the brain and skin. Although much has recently been written about this disease in the neuropathology literature, to our knowledge nothing has appeared in the dermatology literature. We wish to call attention to the unique role dermatologists and dermatopathologists can play in the diagnosis of this disease. We review the condition's clinical, histologic, and ultrastructural features.

Biopsy, Needle↗

[Inhibiting effect of antisense oligodeoxynucleotide of alpha 1(I) Precollagen gene on hypertrophic scar in an animal model].

OBJECTIVE: To study the effect of antisense oligodeoxynucleotide (ODN) of alpha 1(I) precollagen gene on hypertrophic scar in an animal model. METHOD: Hypertrophic scar was explanted in athymic mice. The effect of antisense oligodeoxynucleotide 1 and 2 on the animal model and the inhibition of ODN1 and ODN2 were observed. RESULT: It was showed that antisense oligo (ODN1, 21 bp) located 5'end from the translation start region and antisense oligo (ODN2, 22 bp) between the first exon and the first intron could effectively inhibit scar hypertrophy. However the control groups showed no inhibition. CONCLUSION: Antisense oligodeoxynucleotide could effectively inhibit scar hypertrophy by inhibiting the synthesis of type I collagen protein.

Animals↗

Effects of phenylarsine oxide on expression of heme oxygenase-1 reporter constructs in transiently transfected cultures of chick embryo liver cells.

Heme oxygenase catalyzes the first and rate-controlling step of heme catabolism. Induction of heme oxygenase-1 can be caused by numerous factors, including heme, other metalloporphyrins, transition metal ions, heat shock, ultraviolet light, phorbol esters, sodium arsenite, and phenylarsine oxide (PAO). Induction of this enzyme may protect cells from oxidative damage. Using heme oxygenase-1 promoter/reporter gene constructs, we have previously reported that the sodium arsenite-mediated induction of heme oxygenase-1 in chick embryo liver cells and chicken hepatoma (LMH) cells involves an AP-1 element. We have now investigated whether the PAO-mediated induction of heme oxygenase-1 also involves an AP-1 element. Primary cultures of chick embryo liver cells were transiently transfected with heme oxygenase-1 promoter/reporter gene constructs, treated with PAO, and reporter gene activities were measured. We found that the PAO-mediated increase in reporter gene activity was dose- and time-dependent. This activity was decreased by prior treatment with N-acetylcysteine. Studies with mutated constructs showed that both an AP-1 element and a metal responsive element are involved in the PAO-mediated induction of the heme oxygenase-1 reporter construct. Electrophoretic mobility shift assays showed that nuclear proteins from PAO-treated cells had increased binding to an AP-1 probe, and that this increase was abrogated by N-acetylcysteine. These findings support the hypothesis that the PAO-mediated induction of heme oxygenase-1 is caused by activation of AP-1 and MRE/cMyc elements and may involve nuclear proteins whose states of phosphorylation determine binding to regulatory elements, and thus the level of expression of heme oxygenase-1.

Acetylcysteine↗

Dichlorobis(1-methyl-1H-benzimidazole-N3)-cobalt(II).

The metal atom in the title complex, [CoCl2(C8H8N2)2], has a slightly distorted tetrahedral coordination involving two Cl- ions and two N atoms from the aromatic groups. The dihedral angle between the planes of the two 1-methylbenzimidazole ligands is 117.7 (7) degrees.

Cobalt↗

A potassium sodium double salt of metavanadate, KNa(VO3)2.

Potassium sodium metavanadate, KNa(VO3)2, crystallizes with the pyroxene structure and is made up of VO4 tetrahedral chains, NaO6 octahedra and KO8 dodecahedra. The chains of corner-sharing VO4 tetrahedra are crosslinked through the NaO6 octahedra and KO8 dodecahedra to form a three-dimensional structure with the K+ and Na+ cations, which lie on twofold axes, situated in the void space. The coordination around the Na+ ion is close to normal octahedral, while the O atoms coordinated to the K+ ion are arranged approximately in a dodecahedral fashion.

Crystallization↗

(C2H10N2)[Co(H2O)6](HPO4)2: a supramolecular three-dimensional hydrogen-bonding network.

The title compound, ethylenediammonium hexaaquacobalt bis(hydrogenphosphate), consists of [Co(H2O)6]2+ and [enH2]2+ cations (en is ethylenediamine), and [HPO4]2- anions interconnected by an extensive intermolecular three-dimensional hydrogen-bonding network. The [enH2]2+ cations play an important role in the templating effect. Both [Co(H2O)6]2+ cations are situated on inversion centers. The average Co-O and P-O bond distances are 2.075 (6) and 1.54 (2) A, respectively.

Crystallography, X-Ray↗

Alcohol-induced depersonalization.

BACKGROUND: A case of alcohol-induced depersonalization disorder is presented. The subject had experienced several depersonalization states following the consumption of alcohol rather than from a psychogenic etiology, and the episodes were transient, not chronic. METHODS: Three quantitative EEG (QEEG) studies were performed on the subject, one during the index depersonalization episode and two subsequent studies when the subject was clinically asymptomatic. RESULTS: Slow wave activity (relative theta power) was significantly increased when symptomatic. This slowing was still present over the occiput 3 days after the symptoms had remitted but was absent 17 days after symptoms had ameliorated. CONCLUSIONS: The time course of EEG slowing suggests a metabolic encephalopathy, a condition which likely contributes to the manifestations of depersonalization syndrome.

Adult↗