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Biomedical subjects

S S Su

Publications and source records attributed to S S Su.

At least 19 recordsLinked to original sources
PubMed2001

Increased levels of tissue plasminogen activator antigen and factor VIII activity in nonvalvular atrial fibrillation: relation to predictors of thromboembolism.

INTRODUCTION: Given that nonvalvular atrial fibrillation (AF)-associated stroke can be either cardioembolic or atherothrombotic, we investigated the relationships between nonvalvular AF and hemostatic factors reflecting intrinsic thrombogenic and atherogenic potentials (tissue plasminogen activator [t-PA] antigen, plasminogen activator inhibitor-1, and factor VIII activity). We also evaluated the clinical applicability of these hemostatic factors by examining whether AF subjects with established clinical or echocardiographic predictors of thromboembolism had higher levels of these factors. METHODS AND RESULTS: Of the 3,212 participants of a Chinese population-based study, 53 subjects (1.7%) with AF were identified. Among the hemostatic factors measured, t-PA antigen (median 12.8 vs 8.1 ng/mL; P < 0.01) and factor VIII activity (median 155% vs 133%; P < 0.05) were significantly higher in AF subjects after adjustment for age and sex. In multivariate analysis, features independently associated with t-PA antigen levels were AF, sex, body mass index, systolic blood pressure, total cholesterol, triglycerides, and left ventricular systolic dysfunction. Features independently associated with factor VIII activity levels included AF, age, and total cholesterol. Levels of both t-PA antigen and factor VIII activity were primarily elevated in AF subjects with predictors of thromboembolism (age > 75 years, hypertension, diabetes, and left ventricular systolic dysfunction), whereas in AF subjects with no thromboembolic predictors, plasma levels of hemostatic factors examined were similar to those without AF. CONCLUSION: We demonstrated that nonvalvular AF was independently associated with increased peripheral levels of t-PA antigen and factor VIII activity. Levels of both hemostatic factors were primarily elevated in AF subjects with predictors of thromboembolism. Whether these hemostatic factors are independently predictive of future thromboembolic events in AF patients requires further investigation.

Adult↗
PubMed2000

A growth curve analysis of stress and adolescent drug use.

The purpose of this paper is to describe and examine one pathway by which adolescent drug use increases during early and mid-adolescence. It draws upon recent research on adolescent stress, drug use, and family processes to describe an important stage of the life course. A chief principle underlying the proposed pathway is that the cumulative effect of stressful life experiences over time can lead to a steeper escalation of drug use in adolescence. Furthermore, based on previous stress research, we propose that this effect may be moderated by factors such as sex, income, family attachment, self-esteem, and mastery. Using 4 years of panel data from the Family Health Study (n = 651 adolescents ages 11-14 during Year 1), we estimate a hierarchical growth curve model that examines the time-varying effects of stressful life events and peer relations on drug use. The results indicate that experiencing a high number of life events over time is related to a significant "growth" of drug use, even after controlling for "growth" due to age or peer relations. In addition, this relationship is moderated by family attachment; high levels of attachment serve to diminish this growth significantly.

Adolescent↗
PubMed1998

Parental substance use disorder, mediating variables and adolescent drug use: a non-recursive model.

AIMS: To develop and test a non-recursive model that examines the effects of parental psychoactive substance use disorder (PSUD) on the reciprocal relationships among stressful life events, family attachment, peer drug use and adolescent drug use. DESIGN: A 3-year prospective cohort study followed adolescents from three types of families defined by a parental diagnosis of a psychiatric disorder. SETTING: A large metropolitan area in the upper Midwestern United States. PARTICIPANTS: Seven hundred and seventy-seven 10-16-year-old adolescents from three groups of families: 214 who resided in families in which a parent was diagnosed with PSUD, 181 who resided in families in which a parent was diagnosed with an affective disorder (but no co-morbid PSUD), and 382 who resided in families in which both parents were free of any diagnosable disorder. MEASUREMENTS: Psychiatric disorder was defined by the Structured Clinical Interview for DSM-III-R (SCID). Two follow-up interviews of adolescent respondents were used to measure stressful life events via the Junior High Life Experiences Survey, family attachment via FACES-III and a child-parent strain index, peer drug use, and two self-reported drug use scales designed to measure past-year alcohol use and illicit drug use (e.g. marijuana, cocaine, inhalants). FINDINGS: Nested structural equation models with latent variables revealed that adolescents from PSUD families were at heightened risk of stressful life events, peer drug use, attenuated family attachments and drug use during the first follow-up period. In turn, peer drug use was strongly associated with drug use during the second follow-up period. However, drug use during the first follow-up also led to greater peer drug use and attenuated family attachment during the second follow-up period. The findings support a non-recursive model describing relations among adolescent drug use, peer drug use and family attachment. CONCLUSIONS: Parental psychoactive substance use disorder puts adolescents at significant risk of becoming embedded in a cycle of drug use, associations with drug using peers, and poor family relations.

Adolescent↗
PubMed1998

Stressful life events and adolescent substance use and depression: conditional and gender differentiated effects.

Stressful life circumstances have myriad influences on human health and behavior. Early research focused on the variable distribution of stress and its effects by socioeconomic status, race, and gender. More recent research indicates that variation by age is also an important consideration. For example, adolescent reactions to stressful life events are often inconsistent with adult reactions to similar life situations and transitions. Moreover, since most studies assess only a single outcome--usually depression--they risk classification bias since analyses exclude other potential stress-related outcomes. This paper assesses the gender distinct effects of stressful life events on two outcomes among adolescents, substance use and depressive symptoms. The results of a second-order regression model indicate that life events affect female, but not male, depressive symptoms, especially when self-esteem is low or mastery is high. Furthermore, life events affect substance use when peer drug use is high, or when parental support is low, but this latter effect is limited to female adolescents.

Adolescent↗
PubMed1997

Changes in network characteristics and HIV risk behavior among injection drug users.

Studies indicate that HIV risk behaviors vary greatly among injection drug users (IDUs). The source of such variation is often ascribed to individual differences, but much of it is due to how IDUs are grouped into social networks. Nevertheless, given the turbulent and uncertain lives led by many IDUs, it would not be surprising if their social networks changed substantially over time. We used data from a study of the social networks of IDUs in Chicago and Washington, DC, to examine changes in individual behavior and network characteristics over time. The results indicated few changes in standard network measures, such as density of ties or network size, over time. However, specific network change measures, that is, indicators of movement into and out of networks, showed significant movement of network members over time. Moreover, movement of members into a network significantly predicted a higher likelihood of risky injection drug use over time. We suggest that these movements are indicative of a lack of a stable resource base among IDU networks.

Adolescent↗
PubMed1997

Effect of parental mental health status on adolescents' dietary behaviors.

PURPOSE: The purpose of this study was to explore whether adolescents of substance-abusing and depressed parents were more likely to have poor dietary behaviors than those in the health comparison families. METHODS: The sample consisted of 841 adolescents in families of substance-abusing parents, depressed parents, and parents without a diagnosable psychiatric disorder. All adolescents were given a food frequency questionnaire. RESULTS: Adolescents whose parents had substance abuse disorder had lower intakes of fruits and higher intakes of high fat foods, and also ate more frequently at fast-food restaurants and purchased more snacks. Adolescents whose parents were depressed had lower intakes of all food groups. Mother's mental health status impacted more on adolescents' dietary behaviors than did the father's mental health status. CONCLUSION: This research suggests that at-risk behaviors among youth of psychiatrically impaired parents may extend to food behaviors.

Adolescent↗
PubMed1996

A nitrogen starvation-induced dormant G0 state in fission yeast: the establishment from uncommitted G1 state and its delay for return to proliferation.

Fission yeast cells either remain in the mitotic cell cycle or exit to meiotic sporulation from an uncommitted G1 state dependent on the presence or absence of nitrogen source in the medium (Nurse and Bissett, 1981). We examined how heterothallic haploid cells, which cannot sporulate, behave under nitrogen-starvation for longer than 25 days at 26 degrees C. These cells were shown to enter a stable state (designated the dormant G0) with nearly full viability. Maintaining the dormant cells required glucose, suggesting that the cells remained metabolically active although cell division had ceased. They differed dramatically from mitotic and uncommitted G1 cells in heat resistance, and also in cytoplasmic and nuclear morphologies. After nitrogen replenishment, the initial responses of dormant G0 cells were investigated. The kinetics for reentry into the proliferative state were delayed considerably, and the changes in cell shape were enhanced particularly for those recovering from extended nitrogen starvation. A part of the delay could be accounted for by the duration of nuclear decondensation and cell elongation for the first cell division.

Cell Division↗
PubMed1993

Molecular characterization of the yeast meiotic regulatory gene RIM1.

In the yeast Saccharomyces cerevisiae, genetic studies suggest that the RIM1 gene encodes a positive regulator of meiosis. rim1 mutations cause reduced expression of IME1, which is required for expression of many meiotic genes, and thus lead to a partial defect in meiosis and spore formation. We report the sequence of RIM1 and functional analysis of its coding region. The RIM1 gene product (RIM1) contains three regions similar to C2H2 zinc fingers. Serine substitutions for cysteine in each of the putative zinc fingers abolish RIM1 function. The carboxyl-terminus of RIM1 is enriched in acidic amino acids and is required for full RIM1 activity. RIM1 also contains two putative cAMP-dependent protein kinase (cAPK) phosphorylation sites. At one site, substitution of alanine for serine does not affect RIM1 activity; at the other site, this substitution impairs activity. This analysis of RIM1 suggests that the protein may function as a transcriptional activator. We have used the cloned RIM1 gene to create a complete rim1 deletion. This null allele, like previously isolated rim1 mutations, causes a partial meiotic defect. In addition to RIM1, maximum IME1 expression requires the MCK1 and IME4 gene products. Defects associated with rim1, mck1, and ime4 mutations in expression of a meiotic reporter gene (ime2-lacZ) and in sporulation are additive. These findings suggest that RIM1 acts independently of MCK1 and IME4 to stimulate IME1 expression.

Amino Acid Sequence↗
PubMed1993

Identification of functionally related genes that stimulate early meiotic gene expression in yeast.

Meiosis and spore formation in the yeast Saccharomyces cerevisiae are associated with increased expression of sporulation-specific genes. One of these genes, IME2, encodes a putative protein kinase that is a positive regulator of other sporulation-specific genes. We have isolated mutations that cause reduced expression of an ime2-lacZ fusion gene. We found mutations in IME1, a known positive regultor of IME2, and MCK1, a known positive regulator of IME1. We also isolated recessive mutations in 12 other genes, which we designate RIM (Regulator of IME2) genes. Our analysis indicates that the defects in rim1, rim8, rim9 and rim13 mutants are a consequence of diminished IME1 expression and can be suppressed by expression of IME1 from the heterologous ACT1 promoter. These rim mutations also reduced expression of an ime1-HIS3 fusion, in which the HIS3 gene is expressed from the IME1 promoter, and caused reduced levels of IME1 RNA. Although the rim1, rim8, rim9 and rim13 mutant phenotypes are similar to those of mck1 mutants, we found that the defects in ime2-lacZ expression and sporulation of the mck1 rim double mutants were more severe than either single mutant. In contrast, the defects of the rim rim double mutants were similar to either single mutant. The rim1, rim8, rim9 and rim13 mutants also display slow growth at 17 degrees and share a smooth colony morphology that is not evident in mck1 mutants or isogenic wild-type strains. We suggest that RIM1, RIM8, RIM9 and RIM13 encode functionally related products that act in parallel to MCK1 to stimulate IME1 expression.

Cloning, Molecular↗
PubMed1990

Role of IME1 expression in regulation of meiosis in Saccharomyces cerevisiae.

Two signals are required for meiosis and spore formation in the yeast Saccharomyces cerevisiae: starvation and the MAT products a1 and alpha 2, which determine the a/alpha cell type. These signals lead to increased expression of the IME1 (inducer of meiosis) gene, which is required for sporulation and sporulation-specific gene expression. We report here the sequence of the IME1 gene and the consequences of IME1 expression from the GAL1 promoter. The deduced IME1 product is a 360-amino-acid protein with a tyrosine-rich C-terminal region. Expression of PGAL1-IME1 in vegetative a/alpha cells led to moderate accumulation of four early sporulation-specific transcripts (IME2, SPO11, SPO13, and HOP1); the transcripts accumulated 3- to 10-fold more after starvation. Two sporulation-specific transcripts normally expressed later (SPS1 and SPS2) did not accumulate until PGAL1-IME1 strains were starved, and the intact IME1 gene was not activated by PGAL1-IME1 expression. In a or alpha cells, which lack alpha 2 or a1, expression of PGAL1-IME1 led to the same pattern of IME2 and SPO13 expression as in a/alpha cells, as measured with ime2::lacZ and spo13::lacZ fusions. Thus, in wild-type strains, the increased expression of IME1 in starved a/alpha cells can account entirely for cell type control, but only partially for nutritional control, of early sporulation-specific gene expression. PGAL1-IME1 expression did not cause growing cells to sporulate but permitted efficient sporulation of amino acid-limited cells, which otherwise sporulated poorly. We suggest that IME1 acts primarily as a positive regulator of early sporulation-specific genes and that growth arrest is an independent prerequisite for execution of the sporulation program.

Amino Acid Sequence↗
PubMed1989

Isolation and characterization of the Escherichia coli mutL gene product.

The Escherichia coli mutL gene product has been purified to near homogeneity from an overproducing clone. The mutL locus encodes a polypeptide of 70,000 daltons as determined by denaturing gel electrophoresis. The native molecular weight of MutL protein as calculated from the sedimentation coefficient of 5.5 S and Stokes radius of 61 A is 139,000 daltons, indicating that MutL exists as a dimer in solution. In addition to its ability to complement methyl-directed DNA mismatch repair in mutL-deficient cell-free extracts, DNase I protection experiments demonstrate that the purified MutL protein interacts with the MutS-heteroduplex DNA complex in the presence of ATP.

Bacterial Proteins↗
PubMed1989

Gap formation is associated with methyl-directed mismatch correction under conditions of restricted DNA synthesis.

A covalently closed, circular heteroduplex containing a G-T mismatch and a single hemimethylated d(GATC) site is subject to efficient methyl-directed mismatch correction in Escherichia coli extracts when repair DNA synthesis is severely restricted by limiting the concentration of exogenously supplied deoxyribonucleoside-5'-triphosphates or by supplementing reactions with chain-terminating 2',3'-dideoxynucleoside triphosphates. However, repair under these conditions results in formation of a single-strand gap in the region of the molecule containing the mismatch and the d(GATC) site. These findings indicate that repair DNA synthesis required for methyl-directed correction can initiate in the vicinity of the mispair, and they are most consistent with a repair reaction involving 3'----5' excision (or strand displacement) from the d(GATC) site followed by 5'----3' repair DNA synthesis initiating in the vicinity of the mismatch.

DNA Repair↗
PubMed1989

The impact of changing methods of data collection on the reliability of self-reported drug use of adolescents.

The purpose of this study is to determine the impact of different modes of data collection on the reliability of self-reported drug use of adolescents in a panel study. Adolescents were assigned to four groups based upon the ways they chose to respond to the survey instruments: 1) mailed questionnaires in both years, 2) survey interview in one year and mailed questionnaire in the next year, 3) mailed questionnaire in one year and survey interview in the following year, and 4) survey interview in both years. The quality of the self-reported data was examined in terms of return rates, missing data, internal consistency, and consistency of reported information over time. No significant differences were found between groups, suggesting that the mode of data collection does not affect the reliability of adolescents' self-reports of substance use.

Adolescent↗
PubMed1988

Mismatch-containing oligonucleotide duplexes bound by the E. coli mutS-encoded protein.

The binding of the mutS gene product, a protein involved in at least two E. coli mismatch correction pathways, to a series of synthetic DNA duplexes containing mismatches or mismatch analogues of the purine/pyrimidine type was studied in order to establish whether a correlation exists between the recognition of these mispairs and the efficiency of their correction in vivo. Experiments using nitrocellulose filter binding or band-shift assays revealed that duplexes containing a G/T mismatch or its analogues I/T and DI/T were bound by the protein with affinities correlating to the efficiency of their repair in vivo. In contrast, the A/C mismatch, contained within the same sequence, was bound only poorly, despite being efficiently corrected in vivo. The analogues of the A/C mispair, uncorrected in vivo, were not detectably bound under the conditions of these assays.

Bacterial Proteins↗
PubMed1988

Mispair specificity of methyl-directed DNA mismatch correction in vitro.

To evaluate the substrate specificity of methyl-directed mismatch repair in Escherichia coli extracts, we have constructed a set of DNA heteroduplexes, each of which contains one of the eight possible single base pair mismatches and a single hemimethylated d(GATC) site. Although all eight mismatches were located at the same position within heteroduplex molecules and were embedded within the same sequence environment, they were not corrected with equal efficiencies in vitro. G-T was corrected most efficiently, with A-C, C-T, A-A, T-T, and G-G being repaired at rates 40-80% of that of the G-T mispair. Correction of each of these six mispairs occurred in a methyl-directed manner in a reaction requiring mutH, mutL, and mutS gene products. C-C and A-G mismatches showed different behavior. C-C was an extremely poor substrate for correction while repair of A-G was anomalous. Although A-G was corrected to A-T by the mutHLS-dependent, methyl-directed pathway, repair of A-G to C-G occurred largely by a pathway that is independent of the methylation state of the heteroduplex and which does not require mutH, mutL, or mutS gene products. Similar results were obtained with a second A-G mismatch in a different sequence environment suggesting that a novel pathway may exist for processing A-G mispairs to C-G base pairs. As judged by DNase I footprint analysis, MutS protein is capable of recognizing each of the eight possible base-base mismatches. Use of this method to estimate the apparent affinity of MutS protein for each of the mispairs revealed a rough correlation between MutS affinity and efficiency of correction by the methyl-directed pathway. However, the A-C mismatch was an exception in this respect indicating that interactions other than mismatch recognition may contribute to the efficiency of repair.

Base Composition↗
PubMed1987

Requirement for d(GATC) sequences in Escherichia coli mutHLS mismatch correction.

The involvement of d(GATC) sequences in Escherichia coli DNA mismatch correction was ascertained by analyzing in vitro repair efficiencies of a series of related, covalently closed circular DNA heteroduplexes that contained from zero to four d(GATC) sites. A heteroduplex with four d(GATC) sites was repaired with high efficiency by extracts of E. coli, whereas no significant correction occurred on a closely related molecule lacking such sequences. Heteroduplexes containing one or two d(GATC) sites were corrected at rates between 10% and 93% of that observed for the four-site molecule, but repair efficiency did not correlate in a simple way with the number of sites present. The methylation state at a single d(GATC) sequence was sufficient to direct strandedness of repair, and correction of heteroduplexes containing one or more d(GATC) sites required functional mutH, mutL, and mutS gene products. In addition, DNA repair synthesis dependent on mutH and mutS also required the presence of at least one d(GATC) site. Although mismatch correction was not observed on a covalently closed circular heteroduplex lacking a d(GATC) sequence, such molecules were subject to strand-specific repair if they contained a strand-specific single-strand break. However, this correction reaction did not require mutH, mutL, mutS, or uvrD gene products. Consequently, we have concluded that d(GATC) sequences are directly involved in mismatch correction mediated by the mutHLS system.

Base Sequence↗
PubMed1986

Escherichia coli mutS-encoded protein binds to mismatched DNA base pairs.

The Escherichia coli mutS gene product is involved in mismatch correction in this organism. We have purified a biologically active form of the 97,000 Mr protein to near homogeneity from an overproducing strain. Enzymatic and chemical protection ("footprinting") experiments have demonstrated that mutS-encoded protein specifically binds to DNA regions containing a single base-pair mismatch. The protein displayed variable affinity for the limited set of mismatches tested (G-T greater than G-A approximately equal to A-C greater than T-C).

Bacterial Proteins↗