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At least 19 recordsLinked to original sources
PubMed2002

Electrocardiographic ST segment elevation: a comparison of AMI and non-AMI ECG syndromes.

Chest pain (CP) patients presenting to the ED may manifest electrocardiographic ST segment elevation (STE). AMI (acute myocardial infarction) is a less frequent cause of such abnormality and one of many patterns responsible for ST segment elevation in ED CP patients. We performed a retrospective comparative review of the electrocardiographic features of various STE syndromes, focusing on differences between AMI and non-AMI syndromes. The electrocardiograms (ECGs) of consecutive ED adult CP patients (with 3 serial troponin I determinations) were interpreted by 3 attending emergency physicians. These ECGs with STE represented the study population used for analysis. Various electrocardiographic features such as STE, ST segment depression (STD), STE morphology, anatomic distribution of STE, and the number of leads with STE were recorded; derived values such as total STE, total ST segment deviation, and average STE per lead were calculated. Interobserver reliability concerning STE morphology was determined. AMI was diagnosed by abnormal serum troponin I values (>0.1 mg/dL) followed by a rise and fall of the serum marker; STE diagnoses of non-AMI causes were determined by medical record review. Five hundred ninety-nine CP patients were entered in the study with 212 (35%) individuals showing STE, 55 (26%) with electrocardiographic AMI and 157 (74%) with non-AMI electrocardiographic syndromes. Anatomic location within the AMI group included 32 inferior and inferior variants, 18 anterior and anterior variants, and 5 lateral; non-AMI anatomic locations included 56 inferior and inferior variants, 98 anterior and anterior variants, and 3 lateral; anterior STE occurred significantly more often in non-AMI syndromes. Total STE was 15.3 mm in AMI patients and 7.4 mm in non-AMI patients (P =.0004). The number of leads with STE was not significantly different between the two groups, 3.4 mm in AMI and 4.1 in non-AMI syndromes. ST segment elevation per lead was not significantly different in the 2 groups, 4.4 mm in AMI versus 1.8 mm in non-AMI syndromes. Total ST segment deviation (sum of STE and STD) was significantly greater in AMI syndromes, 17.8 mm in AMI compared with 10.5 mm in non-AMI syndromes (P =.00009). The presence of STD occurred at statistically similar rates in both groups. The morphology of the STE occurred in significantly different rates between AMI and non-AMI patterns, concave more often in non-AMI patterns (P <.00001) and nonconcave more often in AMI (P <.00001). Non-AMI causes of STE account for the majority of electrocardiographic syndromes encountered in ED chest pain patients. These findings alone are not adequate to determine the electrocardiographic cause of the ST segment elevation in chest pain patients. When determining AMI versus non-AMI with the ECG, these various findings should be used in the consideration of the overall clinical picture (history, examination, and electrocardiogram) in chest pain patients with ST segment elevation.

Angina Pectoris↗
PubMed1994

Molecular analysis of cis-regulatory sequences of the alpha-amylase gene in D. melanogaster: a short 5'-flanking region of Amy distal gene is required for full expression of Amy proximal gene.

The structural locus for alpha-amylase (AMY) in Drosophila melanogaster is duplicated and divergently transcribed. These two genes are designated as Amy-p and Amy-d, respectively. We searched for the cis-acting regulatory elements for full expression of the duplicated Amy-p and Amy-d loci, by injecting plasmid constructs containing sequences from the Amy locus into preblastoderm embryos of an AMY-null strain and measuring exogenous AMY activity produced in transformed host larvae (i.e., the transient expression assay). Relative activities of endogenous amylase isozymes, AMY-1 and AMY-3, in extracts of AMY1,3 larvae of a Canton-S are almost the same. However, three independently isolated Amy-p1 constructs with only the 5' upstream regions of Amy-p1 expressed a very low AMY-1 activity. Two other Amy-p1 constructs with the 5' upstream region of Amy-d3 in addition to that of Amy-p1 produced a high activity. Thus, the 5' upstream region of Amy-d3 is necessary for full expression of Amy-p1. In order to locate cis-regulatory elements within the 5' region of Amy-d3, a series of hybrid constructs including this region were tested to locate them. Our results clearly show that the cis-acting regulatory sequences required for full expression of Amy-p1 are located between the base pairs at -304 and -372 upstream of Amy-d3 gene. In other words, only a short region located upstream of Amy-d3 was found to be necessary and sufficient for the full expression of Amy-p1 in addition to its promoter. This region seems also necessary for the expression of Amy-d3.

Animals↗
PubMed1992

Acute myocardial infarction (AMI) in Finland--baseline data from the FINMONICA AMI register in 1983-1985.

The acute myocardial infarction (AMI) register of the FINMONICA study, the Finnish part of the WHO-coordinated multinational MONICA project, operates in the provinces of North Karelia and Kuopio in eastern Finland and in Turku, Loimaa and in communities around Loimaa in southwestern Finland. The AMI register serves as an instrument for the assessment of trends in mortality from coronary heart disease (CHD) and of the incidence and attack rates of AMI among 25-64-year-old residents of the study areas. This report describes the methods used in the FINMONICA AMI register and the findings during the first 3 years of the study, in 1983-1985. The criteria of the multinational WHO MONICA project were used in the classification of fatal events and in the diagnosis of non-fatal definite AMI, but based on the experience within the FINMONICA study, stricter diagnostic criteria than those originally described in the WHO MONICA protocol were used for non-fatal possible AMI. This led to a marked improvement in the comparability of the data from the three study areas with regard to the incidence and attack rates of non-fatal AMI. During the 3-year period the total number of registered events was 6266 among men and 2092 among women. Among men the incidence and attack rates of AMI and mortality from CHD were higher in eastern than in southwestern Finland. Also among women the incidence and attack rates of AMI were higher in eastern than in southwestern Finland, whereas there was no regional difference in mortality from CHD among women. The mortality findings of the FINMONICA AMI Register were in good agreement with the official CHD mortality statistics of Finland.

Adult↗
PubMed2002

AAT-1, a novel testis-specific AMY-1-binding protein, forms a quaternary complex with AMY-1, A-kinase anchor protein 84, and a regulatory subunit of cAMP-dependent protein kinase and is phosphorylated by its kinase.

AMY-1 has been identified by us as a c-Myc-binding protein and was found to stimulate c-Myc transcription activity. AMY-1 was also found to be associated with protein kinase A anchor protein 84/149 (S-AKAP84/AKAP149) in the mitochondria in somatic cells and sperm, suggesting that it plays a role in spermatogenesis. To determine the molecular function of AMY-1, a two-hybrid screening of cDNAs encoding AMY-1-binding proteins was carried out with AMY-1 as a bait using a human testis cDNA library, and a clone encoding a novel protein, AAT-1, was obtained. Three isoforms of AAT-1, AAT-1alpha, -beta, and -gamma, were found to be derived from an alternative splicing of the transcripts of the aat-1 gene, which was mapped at human chromosome 3q13-3q21. AAT-1 was found to be specifically expressed in the testis during the course of spermatogenesis and also to be present in the spermatid and mature sperm, as was AMY-1. AAT-1alpha was found to bind to and be colocalized in mitochondria with AMY-1 in human HeLa and mouse GC-1 cells. Furthermore, AAT-1alpha was found to bind to the N-terminal half of S-AKAP84/AKAP149 in a quaternary complex with AMY-1 and a regulatory subunit (RII) of cAMP-dependent kinase (PKA), in which AAT-1alpha was associated with RII via S-AKAP84/AKAP149, in rat testis and HeLa cells. It was then found that AAT-1alpha weakly stimulated a phosphorylation activity of PKA and also that AAT-1 itself was phosphorylated by PKA in vivo and in vitro. These results suggest that both AAT-1 and AMY-1 play roles in spermatogenesis.

A Kinase Anchor Proteins↗
PubMed2003

Molecular cloning of the mouse AMY-1 gene and identification of the synergistic activation of the AMY-1 promoter by GATA-1 and Sp1.

We have reported that a novel c-Myc binding protein, AMY-1, stimulated the transcription activity of c-Myc and was translocated from the cytoplasm to the nucleus in a c-Myc-dependent manner. AMY-1 works as an inducer of human K562 cell differentiation upon induction of AraC. To characterize the expression or functional importance of AMY-1, the genomic DNA of mouse AMY-1 was cloned and characterized. Both mouse and human genomic DNAs, the latter of which was retrieved from a human DNA database, comprise five exons spanning about 11 kb. To characterize the promoter of the mouse AMY-1 gene, a series of deletion constructs of the region upstream of the first ATG was linked to the luciferase gene, and their luciferase activities were measured in human HeLa and K562 cells. The results showed that Sp1 was essential for AMY-1 expression in both cell lines and that GATA-1 is also necessary in K562 cells. Sp1 in both cell lines and GATA-1 only in K562 cells were identified as proteins binding to these sites by a mobility shift assay. Furthermore, it was found that GATA-1 stimulated AMY-1 expression synergistically with Sp1 in ectopically expressed insect cells and that both proteins were associated in K562 cells.

Amino Acid Sequence↗
PubMed1985

Mouse alpha-amylase loci, Amy-1a and Amy-2a, are closely linked.

We have cloned a contiguous 106 X 10(3) base-pair long stretch of mouse DNA. The isolated chromosomal DNA segment contains the single copy gene Amy-1a that is strongly expressed in the parotid gland and, 23 X 10(3) base-pairs downstream from it, one member of the pancreas-specific Amy-2a oligogene family. At least two of the four Amy-2a genes, including the copy linked to Amy-1a, are efficiently transcribed. The cloned DNA sequences do not appear to specify messenger RNAs other than those encoding alpha-amylase in pancreas, parotid gland or liver. Transcription termination on Amy-1a occurs within 3 X 10(3) base-pairs downstream from the polyadenylation site in both parotid gland and liver, in which this gene is transcribed at different rates from different promoters.

Animals↗
PubMed2001

Electrocardiographic ST-segment elevation: correct identification of acute myocardial infarction (AMI) and non-AMI syndromes by emergency physicians.

OBJECTIVE: To determine the emergency physician's (EP's) ability to identify the cause of ST-segment elevation (STE) in a hypothetical chest pain patient. METHODS: Eleven electrocardiograms (ECGs) with STE were given to EPs; the patient in each instance was a 45-year-old male with a medical history of hypertension and diabetes mellitus with the chief complaint of chest pain. The EP was asked to determine the cause of the STE and, if due to acute myocardial infarction (AMI), to decide whether thrombolytic therapy (TT) would be administered (the patient had no contraindication to such treatment). Rates of TT administration were determined; appropriate TT administration was defined as that occurring in an AMI patient, while inappropriate TT administration was defined as that in the non-AMI patient. RESULTS: Four hundred fifty-eight EPs completed the questionnaire; levels of medical experience included the following: postgraduate year 2-3, 193 (42%); and attending, 265 (58%). The overall rate of correct interpretation of the study ECGs was 94.9% (4,782 correct interpretations out of 5,038 instances). Acute myocardial infarction with typical STE, ventricular paced rhythm, and right bundle branch block were never misinterpreted. The remaining conditions were misinterpreted with rates ranging between 9% (left bundle branch block, LBBB) and 72% (left ventricular aneurysm, LVA). The overall rate of appropriate thrombolytic agent administration was 83% (1,525 correct administrations out of 1,832 indicated administrations). The leading diagnosis for which thrombolytic agent was given inappropriately was LVA (28%), followed by benign early repolarization (23%), pericarditis (21%), and LBBB without electrocardiographic AMI (5%). Thrombolytic agent was appropriately given in all cases of AMI except when associated with atypical STE, where it was inappropriately withheld 67% of the time. CONCLUSIONS: In this survey, EPs were asked whether they would give TT based on limited information (ECG). Certain syndromes with STE were frequently misdiagnosed. Emergency physician electrocardiographic education must focus on the proper identification of these syndromes so that TT may be appropriately utilized.

Bundle-Branch Block↗
PubMed1999

Comparison of commercial Amies transport systems with in-house Amies medium for recovery of Neisseria gonorrhoeae.

Microbiologists are still encumbered by the variable performance of Amies charcoal transport medium in recovery of Neisseria gonorrhoeae. The objective of this study was to evaluate and select a good quality commercial system to replace our in-house preparation. We adsorbed 0.1 ml of a suspension from 30 gonococcal isolates onto each swab type and replaced the swab into the transport medium. We plated the swabs to New York City medium at 0, 24, 48, 72, and 96 h. We compared the survival of each isolate in the commercial Amies transport systems with that in our in-house Amies transport medium. The best recovery was observed with Copan transport systems. Some systems are inadequate and unacceptable for culture of gonococci.

Culture Media↗
PubMedDate not supplied

Additional evidence for the close linkage of amy-1 and amy-2 in the mouse.

The enzyme amylase is produced in large quantities in two mammalian tissues, the pancreas and the parotid salivary gland. A substantial body of biochemical and genetic evidence is consistent with the existence of distinct genes encoding salivary and pancreatic amylases, but testcrosses in mice have indicated that the two putative loci must be very closely linked. We have studied crosses between two pairs of inbred mice that differ with respect to electrophoretic mobility of salivary and pancreatic amylases. Among 343 potentially recombinant chromosomes examined, no recombinants were found. Our data sets an upper limit of 0.87 cM (P = 0.95) for the distance between the salivary and pancreatic loci.

Amylases↗
PubMed1985

Expression of mouse Amy-2a alpha-amylase genes is regulated by strong pancreas-specific promoters.

Three types of Amy-2-related DNA sequences, Amy-2a I, Amy-2a II and Amy-X, exist in the genome of mice of the inbred strain A/J. Amy-2a I and Amy-X are single copy sequences. Amy-2a II occurs as three copies per haploid genome. DNA sequence analysis reveals that both classes of Amy-2a genes specify the same unique pancreatic alpha-amylase mRNA species, since they share common exon sequences. Four independently cloned Amy-2a II isolates were found to be identical in all regions sequenced. This suggests that most, if not all, chromosomal Amy-2a II copies are identical. Amy-X is presumably a pseudogene, since its exon sequences, which are distinct from those of Amy-2a, are not detected in pancreatic alpha-amylase mRNA. We have determined the transcriptional activities of the Amy-2a genes by mapping in vitro elongated nascent transcripts to Amy-2a restriction fragments. Transcription initiation occurs at or close to the cap site. The expression of Amy-2a in vivo is under control of strong promoters, which are active exclusively in the pancreas. The accumulation of alpha-amylase mRNA in cells of the exocrine pancreas is regulated mainly at the transcriptional level. We have searched for pancreatic transcripts of Amy-1a, which specifies both parotid gland and liver-type alpha-amylase mRNAs. Surprisingly, the weak Amy-1a promoter, which directs the synthesis of the mRNA containing the liver-type leader sequence, also is active in the pancreas and, hence, in all alpha-amylase-producing tissues.

Animals↗
PubMed2004

Sequence and binding activity of the autolysin-adhesin Ami from epidemic Listeria monocytogenes 4b.

Ami is an autolytic amidase from Listeria monocytogenes that is targeted to the bacterial surface via its C-terminal cell wall anchoring (CWA) domain. We recently showed that the CWA domain from Ami of L. monocytogenes EGD (serovar 1/2a) (Ami 1/2a) mediated bacterial binding to mammalian cells. Here we studied the sequence and binding properties of Ami from CHUT 82337 (serovar 4b) (Ami 4b). The Ami 4b polypeptide is predicted to be 770 amino acids long (compared with the 917 amino acids of Ami 1/2a from EGD). Ami 1/2a and Ami 4b are almost identical in the N-terminal enzymatic domain (approximately 98% amino acid identity), but the sequence is poorly conserved in the C-terminal CWA domain, with only approximately 54% amino acid identity and eight GW modules in Ami 1/2a compared with six GW modules in Ami 4b. The purified Ami 4b CWA domain efficiently bound serovar 4b bacterial cells and only poorly bound serovar 1/2a bacterial cells. The Ami 4b CWA domain was also significantly less able to bind Hep-G2 human hepatocytic cells than the Ami 1/2a CWA domain. We sequenced the ami regions encoding CWA domains of reference strains belonging to the 12 L. monocytogenes serovars. The phylogenic tree constructed from the sequences yielded a binary division into group I (serovars 1/2a, 1/2b, 1/2c, 3a, 3b, 3c, and 7) and group II (serovars 4a, 4b, 4c, 4d, and 4e). This is the first direct evidence of divergence between serovars 1/2a and 4b in a gene involved in the adhesion of L. monocytogenes to mammalian cells, as well as the first demonstration of allelic polymorphism correlated with the somatic antigen in this species.

Adhesins, Bacterial↗