Biomedical subjects

Yi Xu

Publications and source records attributed to Yi Xu.

At least 91 records · Page 5Linked to original sources

PubMed2004

[Investigation on emerging rate and prevalence of male homosexuality in Hangzhou City].

OBJECTIVE: To understand prevalence of male homosexuality in Hangzhou, Zhejiang Provicne of China. METHODS: To investigate emerging rate of male homosexuality and infer its prevalence in public gathering by observation at fixed points and questionnaire survey in gay men. RESULTS: There were 2 012.5 male homosexuals taking part in public gatherings, with 95% confidence interval of 1 899 - 2 129, in Hangzhou. Frequency of such activities they took part in was once every 3 - 15 days (11.3 +/- 2.7) days. Each gay man knew 1.51 +/- 0.33 (0 - 6) other male homosexuals who never exposed their sexual orientation. The emerging number of male homosexuals was 5 051.38. CONCLUSION: The emerging rate of male homosexuality was 0.58%, with its prevalence of about 1% - 2% in public gatherings in Hangzhou.

Adult↗

PubMed2004

[Characterizing methods of structure and character for silane film on metal surface].

Surface analysis methods for structure and characters of silane film on metal surface were reviewed in this paper. Many instrumental methods, such as XPS, ATR-FTIR, RA-FTIR, SIMS, ellipsometry, EIS and so on, were applied to characterizing different silane films on different metal base surfaces. According to the research on silane film formation mechanism, silane film state, silane film structure, silane film thickness, silane film corrosion resistance and so on, factors which affect silane film properties were discussed. Various parameters were proposed for characterizing silane film. Merits and defects of various surface analysis methods were expressed. In order to acquire more chemical information, different surface analysis methods can be combined for detection at the same time. Regarding the results from these detection and analysis, new silane treatment technique for metal surface can be optimized and improved greatly. Some other kinds of surface analysis methods were also mentioned in this paper. More advanced researches in the field of silane film analysis on metal surface were prospected.

English Abstract↗

PubMed2003

Angiotensin II-induced MMP-2 release from endothelial cells is mediated by TNF-alpha.

Angiotensin II (ANG II) has been etiologically linked to vascular disease; however, its role in the alterations of endothelial function that occur in vascular disorders is not completely understood. Matrix metalloproteinases (MMPs) and proinflammatory cytokines are involved in the pathological remodeling of blood vessels that occurs in vascular disease. In this study we evaluated the effects of ANG II on tumor necrosis factor (TNF)-alpha and MMP-2 production in endothelial cells. Human umbilical vein endothelial cells (HUVECs) were stimulated with ANG II (0.1-10 microM) for 24 h, in the presence or absence of antagonists of ANG II type 1 (AT(1)R) and type 2 (AT(2)R) receptors, and the production and release of TNF-alpha and MMP-2 were assessed. ANG II increased TNF-alpha mRNA and protein expression and the release of bioactive TNF-alpha. Moreover, ANG II induced MMP-2 release and reduced the secretion of tissue inhibitor of MMP (TIMP)-2 from endothelial cells. To elucidate whether endogenous TNF-alpha could mediate the effects of ANG II on MMP-2 release, cells were pretreated with anti-TNF-alpha neutralizing antibodies or pentoxifylline (an inhibitor of TNF-alpha synthesis). TNF-alpha inhibition prevented the secretion of MMP-2 induced by ANG II. Furthermore, AT(1)R antagonism with candesartan prevented the formation of MMP-2 and TNF-alpha and the reduction of TIMP-2 induced by ANG II. These results indicate that ANG II, via AT(1)R, modulates the secretion of TNF-alpha and MMP-2 from endothelial cells and that TNF-alpha mediates the effects of ANG II on MMP-2 release.

Angiotensin II↗

PubMed2003

Isolation of neural stem cells from the forebrain of deceased early postnatal and adult rats with protracted post-mortem intervals.

Neural stem cells were isolated from deceased early postnatal and adult rats with varying post-mortem intervals. Animals were killed by deep anesthesia and stored in a refrigerator at 4 degrees C for 1-6 days before use. Neurospheres were obtained from the forebrain tissue, including the lateral ventricle in the early postnatal rats, and from the striatal wall of lateral ventricle, including the subventricular zone (SVZ) in adult rats. The number of neurospheres obtained in the primary culture from early postnatal animals was much larger than that from the adult rats. There was no significant difference in the population of neurospheres between the living and the deceased animals at least within 2 days after death. A few neurospheres were still obtainable at 6 days after death in early postnatal animals, but almost no neurospheres were obtained at 5 days after death in the adult rats. The differentiation capacity of neural stem cells in neurospheres was similar between the deceased and the living animals. The rich vascular bed in the SVZ of the lateral ventricle suggests that the vascular architecture might be in part responsible for the survival of the neural stem cells in the deceased animals. Neurosphere cells derived from deceased adult rats survived and differentiated mainly into glial cells in the host spinal cord tissue after transplantation into the injured spinal cord. Therefore, the neural stem cells from deceased animals express the same phenotypes as those from living animals in terms of neurosphere formation, proliferation, and differentiation at least 2 days after death. The neural stem cells from cadavers have great significance in terms of their clinical use as homografts for CNS regeneration.

Animals↗

PubMed2003

A "dock, lock, and latch" structural model for a staphylococcal adhesin binding to fibrinogen.

Gram-positive pathogens such as staphylococci contain multiple cell wall-anchored proteins that serve as an interface between the microbe and its environment. Some of these proteins act as adhesins and mediate bacterial attachment to host tissues. SdrG is a cell wall-anchored adhesin from Staphylococcus epidermidis that binds to the Bbeta chain of human fibrinogen (Fg) and is necessary and sufficient for bacterial attachment to Fg-coated biomaterials. Here, we present the crystal structures of the ligand binding region of SdrG as an apoprotein and in complex with a synthetic peptide analogous to its binding site in Fg. Analysis of the crystal structures, along with mutational studies of both the protein and of the peptide, reveals that SdrG binds to its ligand with a dynamic "dock, lock, and latch" mechanism. We propose that this mechanism represents a general mode of ligand binding for structurally related cell wall-anchored proteins of gram-positive bacteria.

Adhesins, Bacterial↗

PubMed2003

Sub-second isoelectric focusing in free flow using a microfluidic device.

Using a microfabricated chip with a bed volume of 0.2 microL we demonstrate the validity of the scaling laws for molecular mass transport of isoelectric focusing (IEF) in free flow. Nano- or microlitre sample volumes can be concentrated within 430 ms by a factor of up to 400. These very fast performances make the chip applicable to proteomic analysis and for continuous monitoring of biochemical processes.

Angiotensin I↗

PubMed2003

Decorin-binding sites in the adhesin DbpA from Borrelia burgdorferi: a synthetic peptide approach.

Lyme disease is caused by the spirochete Borrelia burgdorferi following transmission from infected Ixodes ticks to human hosts. Following colonization of the skin, spirochetes can disseminate throughout the body, resulting in complications that can include ocular, cardiac, neural, and skeletal disease. We have previously shown that B. burgdorferi expresses two closely related decorin-binding adhesins (DbpA and DbpB) of the MSCRAMM (microbial surface component recognizing adhesive matrix molecule) type that can mediate bacterial attachment to extracellular matrices in the host. Furthermore, three Lys residues in DbpA appear to be critical for the binding of DbpA to decorin. We have now characterized the interaction of DbpA and decorin further by using a synthetic peptide approach. We synthesized a panel of peptides that spanned the DbpA sequence and examined their ability to inhibit the binding of intact DbpA to decorin. From these studies, we identified a decorin-binding peptide that lost this activity if the sequence was either scrambled or if a critical Lys residue was chemically modified. A minimal decorin-binding peptide was identified by examining a set of truncated peptides. One peptide is proposed to contain the primary decorin-binding site in DbpA. By comparing the amino acid sequences of 29 different DbpA homologs from different B. burgdorferi sensu lato isolates, we discovered that the identified decorin-binding sequence was quite variable. Therefore, we synthesized a new panel of peptides containing the putative decorin-binding sequence of the different DbpA homologs. All of these peptides were active in our decorin-binding assay, and consensus decorin binding motifs are discussed.

Adhesins, Bacterial↗

PubMed2003

ATP binding to Rho transcription termination factor. Mutant F355W ATP-induced fluorescence quenching reveals dynamic ATP binding.

Rho transcription termination factor mutant, F355W, showed tryptophan fluorescence intensity approximately twice that of wild-type Rho at equivalent protein concentrations and underwent a decrease in relative fluorescence intensity at 350 nm when 100 microm ATP was added in the presence or absence of RNA. Titration of this fluorescence quenching with varying concentrations of ATP (0-600 microm), where Rho is shown to exist as a hexamer (400 nm Rho), revealed tight and loose ATP-binding sites. Bicyclomycin, a specific inhibitor of Rho, increased the tight ATP binding and was used to calibrate ATP-induced fluorescence quenching by using [gamma-(32)P]ATP filter binding. For the Rho mutant F355W, three tight (K(d)(1) = 3 +/- 0.3 microm) and three loose (K(d)(2) = 58 +/- 3 microm) ATP-binding sites per hexamer were seen on Scatchard analysis in the absence of bicyclomycin and poly(C). In the presence of bicyclomycin, the K(d)(1) changed from 3.0 to 1.4 microm, but K(d)(2) underwent a lesser change. The non-hydrolyzable ATP analogue, gamma-S-ATP, gave a similar profile with three tight (K(d)(1) = 0.2 microm) and three loose (K(d)(2) = 70 microm) ATP-binding sites per hexamer. Adding poly(C) to F355W did not alter the K(d)(1) or K(d)(2) for ATP or for gamma-S-ATP. ADP-induced quenching produced 5.5 loose (K(d) = 92 microm) binding sites in the absence of poly(C), and the binding became weaker (K(d) = 175 microm) in the presence of poly(C). The data suggest that in the presence of ADP Rho has six equivalent nucleotide-binding sites. When ATP was added these sites converted to three tight and three loose binding loci. We propose an alternating ATP site mechanism where ATP binding creates heterogeneity in the ATP binding in adjacent subunits, and we suggest that ATP binding to a neighboring loose site stimulates hydrolysis at a neighboring tight binding site such that all six subunits can be potential "active" sites for ATP hydrolysis. The dynamic nature of the ATP binding to Rho is discussed in the terms of the mechanism of RNA tracking driven by ATP hydrolysis.

Adenosine Diphosphate↗

PubMed2003

[Endovascular stent-assisted angioplasty for atherosclerotic intracranial stenosis, a clinical analysis of 39 cases].

OBJECTIVE: To assess the preliminary outcome of endovascular stent-assisted angioplasty for intracranial stenosis. METHODS: Thirty-nine patients with atherosclerotic intracranial stenosis (19 cases in posterior circulation and 20 in anterior circulation) were treated with endovascular angioplasty using balloon-expandable coronary stents. Follow-up was made for 4 - 24 months. The clinical manifestations were observed and CT, MR, or DSA were conducted before and after the operation. RESULTS: All of the stents were successfully implanted on the first procedure without procedural and periprocedural complications. The mean carotid artery stenosis rate was 73.5 +/- 6.7% before the procedure and 11.2 +/- 4.3% after the procedure. The patients were clinical asymptomatic and neurologically intact. Follow-up angiographies made in 29 patients revealed no restenosis. CONCLUSION: With effective short-term results and helpful in decreasing incidence of stroke, endovascular stenting is safe and feasible for treatment of intracranial stenosis.

Adult↗

PubMed2003

Estrogen reduces angiotensin II-induced nitric oxide synthase and NAD(P)H oxidase expression in endothelial cells.

OBJECTIVE: Angiotensin II (AII) has been shown to increase endothelial NAD(P)H oxidase activity, which is a source of superoxide anion that in turn may induce the formation of peroxynitrite. Estrogen (E2) has been reported to have vascular protective effects. In this study, we hypothesized that E2 reduces the AII-induced expression of NAD(P)H oxidase and peroxynitrite in endothelial cells. METHODS AND RESULTS: Endothelial cells were cultured and stimulated with AII in the absence or presence of E2. Western blots were used to assess nitric oxide synthase (NOS) and NAD(P)H oxidase expression. Immunofluorescence of nitrotyrosine provided evidence of peroxynitrite formation. Our data indicate that AII increased the expression of endothelial NOS, inducible NOS, and NAD(P)H oxidase in a dose-dependent manner, which was attenuated by incubation with either E2, superoxide dismutase, or the AII type 1 receptor (AT1R) inhibitor candesartan. Estrogen as well as superoxide dismutase also inhibited AII-induced AT(1)R expression and nitrotyrosine staining. The effects of E2 on the AII responses were not inhibited by the E2 receptor antagonist ICI-182,780. CONCLUSIONS: AII stimulation of endothelial cells increases expression of NAD(P)H oxidase and NOS, which may contribute to oxidative stress, as evidenced by peroxynitrite formation. E2 inhibits these AII effects, possibly through reduced AT1R expression.

Angiotensin II↗

PubMed2003

Repair of 8 oxoguanine in mammalian cells expressing the Drosophila S3 ribosomal/repair protein.

8-oxo-7,8-dihydroguanine (8-oxoG) is a potent mutagenic lesion that forms at elevated levels in cellular DNA and is repaired with low efficiency in human cells. Unlike its human counterpart, the Drosophila S3 ribosomal/repair protein is endowed with a vigorous 8 oxoG repair activity that is associated to beta,delta-elimination AP lyase activity. We have recently observed that pure GST-tagged Drosophila S3 protein can significantly accelerate the in vitro repair of 8 oxoG performed by human and mouse cell extracts [Cappelli et al., unpublished data]. In this work, we have transfected Chinese hamster cells with mammalian expression vectors containing the Drosophila S3 cDNA. The cells synthesized both S3 mRNA and protein but no improved repair of 8 oxoguanine was observed. Factors important for the proper expression of Drosophila genes in mammalian cells are discussed.

Animals↗

PubMed2003

Certification assays for HIV-1-based vectors: frequent passage of gag sequences without evidence of replication-competent viruses.

A principal concern regarding the safety of HIV-1-based vectors is replication-competent lentivirus (RCL). We have developed two PCR assays for detecting RCL; the first detects recombination between gag regions in the transfer vector and the packaging construct (sensitivity of detection approximately 10-100 copies of target sequence). The second assay uses real-time PCR to detect vesicular stomatitis virus glycoprotein (VSVG) envelope DNA (sensitivity approximately 5-50 VSVG sequences). In an attempt to amplify any RCL, test vectors were used to transduce C8166 and 293 cells, which were then screened weekly for 3 weeks. Psi-gag recombinants were routinely detected (20 of 21 analyses) in four transductions using the RRL-CMV-GFP vector. In contrast, VSVG sequences were detected only once in 21 analyses. Interestingly, p24 levels (as measured by ELISA) were occasionally detectable after 3 weeks of culture. To determine if a true RCL was present, 21-day cell-free medium was used to transduce naïve cells. No evidence of psi-gag or VSVG transfer was detected, indicating that the recombination events were insufficient to reconstitute a true RCL. These findings have important implications for the design and safety of HIV-1-based vectors intended for clinical applications.

Base Sequence↗

PubMed2003

Estrogen modulation of left ventricular remodeling in the aged heart.

OBJECTIVE: To investigate the effects of estrogen on left ventricle (LV) mass and collagen deposition, and on the expression of receptors for estrogen (ER alpha, ER beta) and Ang II (AT(2)R, AT(1)R) in the heart of aged female rats. METHODS: Aged ( approximately 12 months old) intact (n=7), ovariectomized plus placebo (OVX, n=7), and estrogen-replaced (E2, n=6) as well as young ( approximately 3 months old, n=4) female Sprague-Dawley rats were used in this study. After 1 month of treatment, the left ventricular weight/body weight ratio (LVW/BW), changes in myosin heavy chain expression (MHC), matrix metalloproteinase (MMP)-2 activity, the collagen I/III ratio, and the expression of ERs and Ang II receptors in the LV were evaluated. RESULTS: In aged rats, OVX increased LVW/BW associated with a higher expression of beta-MHC isoform, increased collagen I/III ratio, and decreased MMP-2 activity compared to intact rats. Furthermore, the OVX group had a decrease in ERs alpha and beta as well as AT(2)R but an increase in AT(1)R expression. Estrogen replacement prevented the effects of ovariectomy on heart remodeling as well as increased further expression of ER beta and decreased AT(1)R expression. CONCLUSION: Removal of ovarian hormones increased LV remodeling in the aged rat, which could be attenuated by estrogen replacement. Moreover, regulation of Ang II receptor expression could be a mechanism by which estrogen may modulate heart remodeling.

Aging↗

PubMed2003

Human-yeast chimeric repair protein protects mammalian cells against alkylating agents: enhancement of MGMT protection.

Chemotherapeutic DNA alkylating agents are common weapons employed to fight both pediatric and adult cancers. In addition to cancerous cells, nontarget tissues are subjected to the cytotoxicity of these agents, and dose-limiting toxicity in the form of myelosuppression is a frequent result of treatment. One approach to prevent myelosuppression that results from the use of chemotherapeutic agents is to increase the levels of DNA repair proteins in bone marrow cells. Here we report our second successful attempt to create a fusion protein that possesses both direct reversal and base excision repair pathway DNA repair activities. The chimeric protein is composed of the human O(6)-Methylguanine-DNA Methyltransferase (MGMT) and the yeast Apn1 proteins and retains both MGMT and AP endonuclease activities as determined by biochemical analysis. We have also demonstrated that the chimeric protein is able to protect mammalian cells from the DNA alkylating agents 1,3-bis (2-chloroethyl)-1-nitrosourea (BCNU) and methyl methanesulfonate (MMS). The protection by the chimeric protein against BCNU is even greater than MGMT alone, which has potential translational significance given that MGMT is currently in clinical trials. Additionally, we show that the chimeric MGMT-Apn1 protein can protect mammalian cells from dual treatments of BCNU and MMS and that this effect is greater than that provided by MGMT alone. The data support our previous finding that a protein with multiple DNA repair activities can be constructed and that this and other constructs may play an important clinical role in guarding against dose-limiting effects of chemotherapy, particularly in situations of multiple drug use.

Alkylating Agents↗

PubMed2003

Incidence of myocardial infarction in randomized clinical trials of protease inhibitor-based antiretroviral therapy: an analysis of four different protease inhibitors.

Protease inhibitor (PI) therapy for patients infected with the human immunodeficiency virus has been associated with lipid disorders and insulin resistance. We compared the incidence of myocardial infarction (MI) among participants receiving treatment with PIs with or without nucleoside reverse transcriptase inhibitors (nRTIs) to nRTI therapy alone in 30 phase II/III double-blind, randomized studies conducted before 1999 for the first 4 PI drugs. In most trials included in this analysis, participants could receive combination therapy with a PI plus nRTIs in open-label extensions after the blinded phase concluded. Person-years (PY) of follow-up were calculated from treatment initiation to the diagnosis of MI, or to the end of the randomized phases for nRTI-only therapy or to the conclusion of the studies for PI-containing regimens. Separate analyses were conducted for the randomized and the randomized-plus-extension phases. Among 10,986 participants, 7951 (72%) received PI drugs at some point for an average duration of 12 months. There were 10 MIs (1.31/1000 PY) in the randomized phases and 19 MIs (1.63/1000 PY) in the randomized-plus-extension phases. The overall stratified relative risk of MI for PI-containing (1.82 MI/1000 PY) versus nRTI-only (1.05 MI/1000 PY) regimens of 1.69 was not significantly increased (95% confidence interval [CI], 0.54 to 7.48). The absolute difference in MI risk was +0.77 (95% CI, -0.71 to +2.26) MIs/1000 PY. Compared with NRTI-only therapy, patients receiving PI-containing regimens for an average of 1 year did not have significantly more MIs, but the upper bound of the 95% CI indicates there may be up to 2.3 additional MIs per 1000 PY. Although studies with a longer duration of PI therapy are in progress to assess whether a later increase in MI incidence occurs, our analysis did not demonstrate a dramatic increase in MI risk during the first year of PI therapy.

Adult↗

PubMed2003

Cardiac effects of amiloride and of enalapril in the spontaneously hypertensive rat.

OBJECTIVES: To compare the effects of the sodium-hydrogen exchange blocker, amiloride, with those of the angiotensin-converting enzyme inhibitor, enalapril, on cardiac structure and function and intracardiomyocyte calcium concentration ([Ca2+]i) and pH (pHi), in spontaneously hypertensive rats (SHRs). METHODS: Experiments were performed in SHRs treated for 4 weeks with amiloride 7.5 mg/kg per day, enalapril 6.0 mg/kg per day or vehicle, and in Sprague-Dawley rats (SDRs). After haemodynamic measurements were taken, the heart was removed and weighed and hydroxyproline (a marker of collagen content) was assayed. In separate rats, ventricular myocytes were isolated, their size determined, and [Ca2+]i and pHi examined using fluo-3 acetoxymethyl ester and 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein tetrakis acetoxymethyl ester fluorescence, respectively. RESULTS: Left ventricular end-diastolic pressure was increased, and the maximal rates of increase and of decrease in pressure with time in the left ventricle were decreased in SHRs compared with SDRs. Myocytes were larger and hydroxyproline was increased in the left ventricle, but not in the right ventricle of SHRs compared with SDRs. Amiloride and enalapril decreased systolic blood pressure in SHRs similarly, and improved diastolic function in these rats, enalapril more than amiloride. Both agents decreased left ventricular myocyte size to similar extents; however, whereas enalapril decreased the left ventricular hydroxyproline content, amiloride did not. Left ventricular myocytes from SHRs exhibited greater [Ca2+]i and pHi than those from SDRs; enalapril decreased [Ca2+]i more than amiloride, but amiloride decreased pHi more than enalapril. CONCLUSIONS: In SHRs, enalapril prevents left ventricular hypertrophy, collagen deposition, diastolic dysfunction, and increases in [Ca2+]i more effectively than does amiloride. In contrast, the latter prevents the increase in pHi more effectively than enalapril, despite similar reductions in blood pressure. These findings suggest that their effects do not depend solely on blood pressure reduction.

Amiloride↗

PubMed2003

Novel as1 and as2 defects in leaf adaxial-abaxial polarity reveal the requirement for ASYMMETRIC LEAVES1 and 2 and ERECTA functions in specifying leaf adaxial identity.

The shoot apical meristem (SAM) of seed plants is the site at which lateral organs are formed. Once organ primordia initiate from the SAM, they establish polarity along the adaxial-abaxial, proximodistal and mediolateral axes. Among these three axes, the adaxial-abaxial polarity is of primary importance in leaf patterning. In leaf development, once the adaxial-abaxial axis is established within leaf primordia, it provides cues for proper lamina growth and asymmetric development. It was reported previously that the Arabidopsis ASYMMETRIC LEAVES1 (AS1) and ASYMMETRIC LEAVES2 (AS2) genes are two key regulators of leaf polarity. In this work, we demonstrate a new function of the AS1 and AS2 genes in the establishment of adaxial-abaxial polarity by analyzing as1 and as2 alleles in the Landsberg erecta (Ler) genetic background. We provide genetic evidence that the Arabidopsis ERECTA (ER) gene is involved in the AS1-AS2 pathway to promote leaf adaxial fate. In addition, we show that AS1 and AS2 bind to each other, suggesting that AS1 and AS2 may form a complex that regulates the establishment of leaf polarity. We also report the effects on leaf polarity of overexpression of the AS1 or AS2 genes under the control of the cauliflower mosaic virus (CAMV) 35S promoter. Although plants with as1 and as2 mutations have very similar phenotypes, 35S::AS1/Ler and 35S::AS2/Ler transgenic plants showed dramatically different morphologies. A possible model of the AS1, AS2 and ER action in leaf polarity formation is discussed.

Arabidopsis↗

PubMed2003

[Psychologic status and their influencing factors in patients suspected of coronary disease before and after coronary catheterization].

OBJECTIVE: To study the psychologic status and their influencing factors in patients suspected of having coronary disease before and after coronary catheterization. METHODS: A hundred fifty-eight inpatients (125 men, 33 women, mean age 66.1 +/- 9.6 years) who underwent a scheduled coronary catheterization for the first time and fulfilled entry criteria were enrolled. All the patients were examined by Symptom Check List-90 (SCL-90), a standard self-report symptom inventory on present psychologic status, within 24 hours before the coronary catheterization (after the information consent) and the third day after the procedure. RESULTS: (1) Before coronary catheterization, factorial scores of somatization, anxiety and phobic anxiety were higher than norm (P < 0.05 or P < 0.01). After the procedure, only somatization score was higher (P < 0.01). (2) Men had higher scores on obsessive-compulsive and psychotism than women (P < 0.05 and P < 0.01, respectively), however, women had higher scores on phobic anxiety (P < 0.05). (3) Compared with patients having coronary disease, those with angiographically normal coronary arteries seemed to have higher scores of somatization, obsessive-compulsive, interpersonal sensitivity, phobic anxiety, paranoid ideation, psychotism, global severity index and positive symptoms (P < 0.05 or P < 0.01). (4) After the procedure, significantly decreases in obsessive-compulsive, depression, hostility, global severity index and positive symptom severity index (P < 0.05 or P < 0.01) were seen. (5) Patients merely underwent coronary angiography had higher score in phobic anxiety construct than those having had coronary angiography and percutaneous transluminal coronary angioplasty (1.34 +/- 0.38 vs 1.15 +/- 0.23, P < 0.05). (6) When compared with the degree of explanation under informed consent, specific risk was not informed mentioned, a higher score in positive symptom severity index was seen (2.56 +/- 0.48 vs 2.46 +/- 0.37, P = 0.02). (7) Higher score was seen on positive symptom severity index when patients aged 70 years or more (2.62 +/- 0.45) than those under 60 years old (2.47 +/- 0.43, P < 0.05) or between 60 and 69 years old (2.45 +/- 0.40, P < 0.01). CONCLUSIONS: Patients' psychologic symptoms before and after the coronary catheterization seemed to be related to many factors. The most important appeared one was coronary catheterization itself. Women, patients with angiographically normal arteries, those of 70 years old or more were more likely to have elevated psychologic distress. Detail information including specific risk regarding the procedure was not associated with the increase of psychological symptoms. The findings emphasized the importance of psychologic assessment and counseling for patient who had undergone a scheduled coronary catheterization.

Adult↗