[Restenosis after PTCA].
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Angioplasty, Balloon, Coronary↗
Biomedical subjects
C J Michel
Publications and source records attributed to C J Michel.
An evolutionary analytical model of a complementary circular code simulating the protein coding genes, the 5' and 3' regions.
The self-complementary subset T0 = X0 [symbol: see text] ¿AAA, TTT¿ with X0 = ¿AAC, AAT, ACC, ATC, ATT, CAG, CTC, CTG, GAA, GAC, GAG, GAT, GCC, GGC, GGT, GTA, GTC, GTT, TAC, TTC¿ of 22 trinucleotides has a preferential occurrence in the frame 0 (reading frame established by the ATG start trinucleotide) of protein (coding) genes of both prokaryotes and eukaryotes. The subsets T1 = X1 [symbol: see text] ¿CCC¿ and T2 = X2 [symbol: see text] ¿GGG¿ of 21 trinucleotides have a preferential occurrence in the shifted frames 1 and 2 respectively (frame 0 shifted by one and two nucleotides respectively in the 5'-3' direction). T1 and T2 are complementary to each other. The subset T0 contains the subset X0 which has the rarity property (6 x 10(-8) to be a complementary maximal circular code with two permutated maximal circular codes X1 and X2 in the frames 1 and 2 respectively. X0 is called a C3 code. A quantitative study of these three subsets T0, T1, T2 in the three frames 0, 1, 2 of protein genes, and the 5' and 3' regions of eukaryotes, shows that their occurrence frequencies are constant functions of the trinucleotide positions in the sequences. The frequencies of T0, T1, T2 in the frame 0 of protein genes are 49, 28.5 and 22.5% respectively. In contrast, the frequencies of T0, T1, T2 in the 5' and 3' regions of eukaryotes, are independent of the frame. Indeed, the frequency of T0 in the three frames of 5' (respectively 3') regions is equal to 35.5% (respectively 38%) and is greater than the frequencies T1 and T2, both equal to 32.25% (respectively 31%) in the three frames. Several frequency asymmetries unexpectedly observed (e.g. the frequency difference between T1 and T2 in the frame 0), are related to a new property of the subset T0 involving substitutions. An evolutionary analytical model at three parameters (p, q, t) based on an independent mixing of the 22 codons (trinucleotides in frame 0) of T0 with equiprobability (1/22) followed by t approximately 4 substitutions per codon according to the proportions p approximately 0.1, q approximately 0.1 and r = 1 - p - q approximately 0.8 in the three codon sites respectively, retrieves the frequencies of T0, T1, T2 observed in the three frames of protein genes and explains these asymmetries. Furthermore, the same model (0.1, 0.1, t) after t approximately 22 substitutions per codon, retrieves the statistical properties observed in the three frames of the 5' and 3' regions. The complex behaviour of these analytical curves is totally unexpected and a priori difficult to imagine.
Animals↗
[Is there a prognostic indication for PTCA?].
Coronary angioplasty is classically indicated to remove a high grade stenosis of a major coronary vessel supplying a large myocardial territory in a symptomatic patient with proven myocardial ischemia. The coronary anatomy has to be suitable for PTCA to ensure a high success rate for the procedure. PTCA is performed to remove symptoms and myocardial ischemia to improve the prognosis of the patient. In contrast to this, the term "prognostic indication" describes an interventional approach to an angiographically documented high grade stenosis in an asymptomatic patient without proven myocardial ischemia thereby hoping to improve the prognosis of this patient. It has to be expected, that up to 20% of all patients treated by balloon angioplasty and 10% of all stented patients are treated with respect to a "prognostic indication". Until now, there are no statistically significant large-scale studies supporting a benefit of an interventional therapy performed with a "prognostic indication" in asymptomatic patients without ischemia. Nevertheless, some certain subgroups of patients may be candidates for a "prognostic indication" to angioplasty compared to the results of medical therapy. In patients treated interventionally for a "prognostic indication" the acute and long-term individual risk of the underlying coronary disease must be carefully weighted against the risk of the interventional procedure.
Angioplasty, Balloon, Coronary↗
[Can recurrences be mechanically prevented?].
The success of interventional catheter based therapy of coronary artery disease is still limited by a high rate of chronic restenosis. Using alternative mechanical techniques, there is increasing evidence that restenosis can be prevented in certain subsets of patients by optimized balloon angioplasty, DCA and stenting as well as by the combined approach of primary tissue removal with adjunctive stent implantation. This article summarizes the mechanical techniques of restenosis prevention or reduction that have been documented in controlled trials. Additional pharmacologic interventions and possibly genetic and/or radiotherapeutic approaches will be highly important for future reduction of restenosis.
Angioplasty, Balloon, Coronary↗
[Differential interventional therapy of coronary heart disease].
Currently, catheter-based coronary therapy is performed using multiple interventional devices. Conventional balloon dilatation is still the dominating therapeutic modality with sufficient results in the majority of coronary lesions. Several alternative new devices were developed to improve acute results and long-term patency compared to balloon dilatation. With use of these devices (stents, coronary atherectomy, laser angioplasty or high speed rotablator) not every coronary lesion can be successfully treated, but several special indications for a differential indication of each of these systems have been found in randomized trials or clinical use. In this review, potential catheter-based strategies for a differential interventional treatment of patients with coronary artery disease are discussed.
Angioplasty, Balloon, Coronary↗
A circular code in the protein coding genes of mitochondria.
A new maximal circular code X0(MIT) with two permutated maximal circular codes X1(MIT) and X2(MIT) is identified in the protein coding genes of mitochondria. The three subsets of 20 trinucleotides X0(MIT)={ACA, ACC, ATA, ATC, CTA, CTC, GAA, GAC, GAT, GCA, GCC, GCT, GGA, GGC, GGT, GTA, GTC, GTT, TTA, TTC}, X1(MIT) and X2(MIT) are in frame 0 (reading frame), 1 and 2 respectively. X1(MIT) and X2(MIT) are deduced by one and two circular permutations of X0(MIT) respectively. The code X0(MIT) has four important properties: a length of the minimal window to automatically retrieve frame 0 which is equal to five nucleotides; an occurrence probability equal to 6.3 x 10(-5); a low frequency (12% in average) of misplaced trinucleotides in the shifted frames; and an occurrence of four types of nucleotides in the first and second trinucleotide sites but no nucleotide G in the third trinucleotide site. Several biological consequences are presented in the Discussion.
Amino Acids↗
[Late reperfusion in acute myocardial infarct. The importance of the open infarct vessel].
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Coronary Vessels↗
An evolutionary model of a complementary circular code.
The subset X0 = [sequence: see text] of 20 trinucleotides has a preferential occurrence in frame 0 (a reading frame established by the ATG start trinucleotide) of protein (coding) genes of both prokaryotes and eukaryotes. This subset X0++ has the rarity property (6 x 10(-8)) to be a complementary maximal circular code with two permutated maximal circular codes X1 and X2 in frames 1 and 2 respectively (frame 0 shifted by one and two nucleotides respectively in the 5'-3' direction). X0 is called a C3 code. A quantitative study of these three subsets X0, X1 and X2 in the three frames 0, 1 and 2 of eukaryotic protein genes shows that their occurrence frequencies are constant functions of the trinucleotide positions in the sequences. The frequencies of X0, X1 and X2 in frame 0 of the eukaryotic protein genes are 48.5%, 29% and 22.5% respectively. These properties are not observed in the 5' and 3' regions of eukaryotes where X0, X1 and X2 occur with variable frequencies around the random value (1/3). Several frequency asymmetries unexpectedly observed, e.g. the frequency difference between X1 and X2 in the frame 0, are related to a new property of the C3 code X0 involving substitutions. An evolutionary model at three parameters (p, q, k) based on an independent mixing of the 20 codons (trinucleotides in frame 0) of X0 with equiprobability (1/20) followed by k approximately 5 substitutions per codon in the three codon sites in proportions p approximately 0.1, q approximately 0.1 and r = 1-p-q approximately 0.8 respectively, retrieves the frequencies of X0, X1 and X2 observed in the three frames of protein genes and explains these asymmetries.
Animals↗
[Intracoronary dipyridamole reduces the incidence of acute coronary vessel occlusion in percutaneous transluminal coronary angioplasty--a prospective randomized study].
Even in the era of coronary stenting, acute coronary artery occlusion continues to represent a significant limitation of percutaneous transluminal coronary angioplasty (PTCA). Despite application of heparin and aspirin, abrupt vessel closure still occurs in 2-8%, depending on the definition applied. Especially patients receiving PTCA for acute coronary syndromes are at high risk for abrupt vessel closure. The formation of an intracoronary thrombus plays a central role in the pathogenesis of abrupt vessel closure. Dipyridamole induces dilatation of coronary arteries and prevents platelet aggregation by a mechanism that differs from that of aspirin. The primary purpose of the study was to evaluate whether adjunctive local intracoronary therapy with dipyridamole could reduce the incidence of coronary artery occlusion following PTCA. Secondary endpoints were defined as myocardial infarction, necessity for bypass grafting, and death. In 939 PTCA procedures performed for stable angina and in 155 angioplasty procedures for acute coronary syndromes (unstable angina, acute myocardial infarction), patients were randomized to receive conventional pretreatment consisting of heparin 15,000 I.E. and aspirin 500 mg i.v. or additional intracoronary infusion of dipyridamole (0.5 mg/kg body weight). Dipyridamole was applied in 550 interventions (455 interventions in men, 95 interventions in women, age = 59.2 +/- 8.4; 74 emergency procedures); conventional pretreatment was performed in 544 interventions (444 interventions in men, 100 interventions in women, age 58.3 +/- 7.9; 81 emergency procedures). Intracoronary application of dipyridamole resulted in a significant reduction in the incidence of abrupt vessel closure following PTCA. This significant reduction was observed in patients presenting with stable ischemia as well as in patients receiving PTCA for acute coronary syndromes. Concerning secondary end points, intracoronary application of dipyridamole did not affect the need for bypass grafting or the incidence of death following PTCA. Intracoronary application of dipyridamole was associated with a reduction in the incidence of myocardial infarction following PTCA which, however, failed to reach significance.
Adult↗
[Acute coronary vessel occlusion after PTCA--possibility of risk stratification using quantitative coronary angiography, clinical determinants and laboratory chemistry parameters].
Abrupt vessel closure of the dilated vessel continues to represent a significant limitation of coronary angioplasty. Despite increasing operator experience and improved technology, abrupt vessel closure continues to represent the most important complication of balloon angioplasty. Intracoronary stent implantation and pharmaceutical blockade of the GPIIb/IIIa receptor serve as effective tools in the prevention of abrupt vessel closure without completely resolving this problem. About 50% of patients presenting with abrupt vessel closure exhibit additional complications including myocardial infarction, necessity of CABG or death occurring in up to 10% of acute occlusions. The purpose of this study is to evaluate if quantitative coronary angiography and assessment of clinical and laboratory data allows risk stratification concerning the probability of abrupt vessel closure. PTCA in the setting of acute coronary syndrome is associated with a markedly increased risk of abrupt vessel closure, indicating that different risk factors may contribute to the development of abrupt vessel closure in patients presenting with stable angina or acute coronary insufficiency syndromes. 798 uncomplicated PTCA procedures for stable angina pectoris were compared with 68 interventions that were complicated by abrupt vessel closure. Furthermore, 133 successful angioplasty procedures for acute coronary syndromes defined as acute myocardial infarction or unstable angina pectoris were matched with 31 procedures for acute coronary syndromes with consecutive abrupt vessel closure. In patients presenting with stable angina pectoris stenosis length, stenosis eccentricity, minimal lumen diameter, degree of the stenosis after angioplasty, female gender, and fibrinogen could be defined as independent predictors of abrupt vessel closure. In acute coronary syndromes, only minimal lumen diameter, recanalization of completely occluded coronary arteries and fibrinogen were associated with an increased risk of abrupt vessel closure.
Aged↗
A code in the protein coding genes.
A statistical analysis with 12,288 autocorrelation functions applied in protein (coding) genes of prokaryotes and eukaryotes identifies three subsets of trinucleotides in their three frames: T0 = X0 [symbol: see text] {AAA, TTT} with X0 = {AAC, AAT, ACC, ATC, ATT, CAG, CTC, CTG, GAA, GAC, GAG, GAT, GCC, GGC, GGT, GTA, GTC, GTT, TAC, TTC} in frame 0 (the reading frame established by the ATG start trinucleotide), T1 = X1 [symbol: see text] {CCC} in frame 1 and T2 = X2 [symbol: see text] {GGG} in frame 2 (the frames 1 and 2 being the frame 0 shifted by one and two nucleotides, respectively, to the right). These three subsets are identical in these two gene populations and have five important properties: (i) the property of maximal (20 trinucleotides) circular code for X0 (resp. X1, X2) allowing to retrieve automatically the frame 0 (resp. 1, 2) in any region of the gene without start codon; (ii) the DNA complementarity property C (e.g. C(AAC) = GTT): C(T0) = T0, C(T1) = T2 and C(T2) = T1 allowing the two paired reading frames of a DNA double helix simultaneously to code for amino acids; (iii) the circular permutation property P (e.g. P(AAC) = ACA): P(X0) = X1 and P(X1) = X2 implying that the two subsets X1 and X2 can be deduced from X0; (iv) the rarity property with an occurrence probability of X0 = 6 x 10(-8); and (v) the concatenation properties in favour of an evolutionary code: a high frequency (27.5%) of misplaced trinucleotides in the shifted frames, a maximum (13 nucleotides) length of the minimal window to retrieve automatically the frame and an occurrence of the four types of nucleotides in the three trinucleotide sites. In Discussion, a simulation based on an independent mixing of the trinucleotides of T0 allows to retrieve the two subsets T1 and T2. Then, the identified subsets T0, T1 and T2 replaced in the 2-letter genetic alphabet {R, Y} (R = purine = A or G, Y = pyrimidine = C or T) allow to retrieve the RNY model (N = R or Y) and to explain previous works in the alphabet {R, Y}. Then, these three subsets are related to the genetic code. The trinucleotides of T0 code for 13 amino acids: Ala, Asn, Asp, Gln, Glu, Gly, Ile, Leu, Lys, Phe, Thr, Tyr and Val. Finally, a strong correlation between the usage of the trinucleotides of T0 in protein genes and the amino acid frequencies in proteins is observed as six among seven amino acids not coded by T0, have as expected the lowest frequencies in proteins of both prokaryotes and eukaryotes.
Animals↗
[Interventional therapy in acute myocardial infarct].
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Angioplasty, Balloon, Coronary↗
[Indications and limits of conventional revascularization methods in coronary heart disease].
The number of cardiologic patients undergoing invasive diagnostic catheterization is rapidly increasing. Due to more liberal and extensive indications for invasive diagnosis patients in relatively unfavorable clinical condition (e.g., elderly patients with severe extracardial disease, patients status post CABG) are being catheterized and, if suitable and indicated, undergo revascularization procedures. With rapidly increasing procedural skill of cardiovascular surgeons and invasive cardiologists even high-risk patients with severe coronary artery disease or underlying illness, who were classically excluded from surgical or catheter-invasive revascularization, are now being treated more aggressively. The changing indications for diagnostic catheterization and significant changes in the different modes of revascularization--operative bypass-surgery or interventional procedures--have led to continuous changes in the differential indications for these invasive therapeutic strategies. This article reviews and discusses the currently accepted indications for surgical and interventional revascularization as well as the limitations of these procedures.
Adult↗
A complementary circular code in the protein coding genes.
Recently, shifted periodicities 1 modulo 3 and 2 modulo 3 have been identified in protein (coding) genes of both prokaryotes and eukaryotes with autocorrelation functions analysing eight of 64 trinucleotides (Arquès et al., 1995). This observation suggests that the trinucleotides are associated with frames in protein genes. In order to verify this hypothesis, a distribution of the 64 trinucleotides AAA,..., TTT is studied in both gene populations by using a simple method based on the trinucleotide frequencies per frame. In protein genes, the trinucleotides can be read in three frames: the reading frame 0 established by the ATG start trinucleotide and frame 1 (resp. 2) which is the frame 0 shifted by 1 (resp. 2) nucleotide in the 5'-3' direction. Then, the occurrence frequencies of the 64 trinucleotides are computed in the three frames. By classifying each of the 64 trinucleotides in its preferential occurrence frame, i.e. the frame associated with its highest frequency, three subsets of trinucleotides can be identified in the three frames. This approach is applied in the two gene populations. Unexpectedly, the same three subsets of trinucleotides are identified in these two gene populations: Tzero = Xzero [symbol: see text] {AAA,TTT} with Xzero = {AAC,AAT,ACC,ATC,ATT, CAG,CTC,CTG,GAA,GAC,GAG, GAT,GCC,GGC,GGT,GTA,GTC,GTT,TAC,TTC} in frame 0, T1 = X1 [symbol: see text] {CCC} in frame 1 and T2 = X2 [symbol: see text] {GGG} in frame 2, each subset Xzero, X1 and X2 having 20 trinucleotides. Surprisingly, these three subsets have five important properties: (i) the property of maximal circular code for Xzero (resp. X1, X2) allowing the automatical retrieval of frame 0 (resp. 1, 2) in any region of a protein gene model (formed by a series of trinucleotides of Xzero) without using a start codon; (ii) the DNA complementarity property C (e.g. C(AAC) = GTT): C(T0) = T0, C(T1) = T2 and C(T2) = T1 allowing the two paired reading frames of a DNA double helix simultaneously to code for amino acids; (iii) the circular permutation property P (e.g. P(AAC) = ACA): P(Xzero) = X1 and P(X1) = X2 implying that the two subsets X1 and X2 can be deduced from Xzero; (iv) the rarity property with an occurrence probability of Xzero equal to 6 x 10(-8); and (v) the concatenation property with: a high frequency (27.5%) of misplaced trinucleotides in the shifted frames, a maximum (13 nucleotides) length of the minimal window to automatically retrieve the frame and an occurrence of the four types of nucleotides in the three trinucleotides sites, in favour of an evolutionary code. In the Discussion, the identified subsets Tzero, T1 and T2 replaced in the three two-letter genetic alphabets purine/pyrimidine, amino/ceto and strong/weak interaction, allow us to deduce that the RNY model (R = purine = A or G, Y = pyrimidine = C or T, N = R or Y) (Eigen & Schuster, 1978) is the closest two-letter codon model to the trinucleotides of Tzero. Then, these three subsets are related to the genetic code. The trinucleotides of Tzero code for 13 amino acids: Ala, Asn, Asp, Gln, Glu, Gly, Ile, Leu, Lys, Phe, Thr, Tyr and Val. Finally, a strong correlation between the usage of the trinucleotides of Tzero in protein genes and the amino acid frequencies in proteins is observed as six among seven amino acids not coded by Tzero, have as expected the lowest frequencies in proteins of both prokaryotes and eukaryotes.
Amino Acids↗
Identification of several types of periodicities in the collagens and their simulation.
The collagens constitute an important population of proteins providing the structural support in vertebrate tissues A collagen is mainly based on a series of tripeptides of the type GX1X2 (G = Glycine, X1 and X2 being any residues). The nine amino acids occurring with significant frequencies in the X1 and X2 residue sites and G form the reduced protein alphabet Q = [A,D,E,G,K,L,P,Q,R,S] (A = Alanine, D = Aspartic acid, E = Glutamic acid, K = Lysine, L = Leucine, P = Proline, Q = Glutamine, R = Arginine, S = Serine). Surprisingly, the method based on the autocorrelation function w(X)iw' analysing the probability that an amino acid w' in Q occurs any i residues X after an amino acid w in Q (called i-motif w(X)iw'), identifies six types of modulo 3 periodicities in collagens: three basic types 0, 1 and 2 modulo 3 and three combined types 0,1, 0,2 and 1,2 modulo 3. Furthermore, the classification of these 100 i-motifs according to the types of periodicities shows several strong relations between four sub-sets of Q [G], [A,D,P,S], [E,L] and [K,Q,R]. Then, these relations allow the construction of a simple automaton for the generation of model collagen sequences. Indeed, this automaton can simulate the six types of periodicities and it retrieves the types of periodicities for almost all i-motifs. Finally, the autocorrelation function based on the sub-set [K,Q,R] identifies segments of 18 amino acids in collagens which may correspond to the exons (segments of genes of 54 nucleotides) coding for those collagens.
Algorithms↗
[Thrombolysis in acute myocardial infarct].
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Angioplasty, Balloon, Coronary↗
Analytical solutions of the dinucleotide probability after and before random mutations.
The mutation process is a classical evolutionary genetic process mainly based on the (random) substitutions of one base (A = Adenine, C = Cytosine, G = Guanine, T = Thymine) for another. Two analytical solutions derived here allow us to analyse in genes the occurrence probabilities of motifs (e.g. dinucleotides) after substitutions (in the evolutionary sense: from the past to the present) and, unexpectedly, also before substitutions (after back substitutions, in the inverse evolutionary sense: from the present to the past). We generalize on the alphabet [A, C, G, T] of the analytical solutions and of the properties derived on the alphabet [R, Y] (R = purine = A or G, Y = pyrimidine = C or T). Application of the theory is based on the analytical solution giving the probabilities of the 16 dinucleotides AA, ..., TT in the protein (coding) genes of (nuclear) eukaryotes, viruses and prokaryotes and in (eukaryotic) introns after back substitutions (called primitive genes). After back substitutions, four of 16 dinucleotides--CG, TA, GT and AC--occur with low probabilities in each of these four primitive gene populations, except for CG in the primitive prokaryotic protein genes. In the primitive eukaryotic protein genes, the dinucleotide AT has also a significant low probability. We present the properties of the two analytical solutions, and the functions which may have these five dinucleotides in primitive genes are described in terms of biological signals.
Animals↗
Identification and simulation of shifted periodicities common to protein coding genes of eukaryotes, prokaryotes and viruses.
The distribution of nucleotides in protein coding genes is studied with autocorrelation functions. The autocorrelation function YRY(N)iYRY, analysing the occurrence probability of the i-motif YRY(N)iYRY (two motifs YRY separated by any i bases N, R = purine = Adenine or Guanine, Y = pyrimidine = Cytosine or Thymine, N = R or Y) in the protein coding genes of eukaryotes, prokaryotes and viruses, reveals the classical periodicity 0 modulo 3 associated with the normal frame 0 (maximal values of the function at i = 0, 3, 6, etc). The specification of YRY(N)iYRY on the alphabet [A, C, G, T] leads to 64 i-motifs: CAC(N)iCAC, CAC(N)iCAT, ..., TGF(N)iTGT. The 64 autocorrelation functions associated with these 64 i-motifs in protein coding genes have all the periodicity modulo 3, but, surprisingly, not always the expected periodicity 0 modulo 3. Two new types of periodicities are identified: a periodicity 1 modulo 3 associated with the shifted frame +1 (maximal values of the function at i = 1, 4, 7, etc) and a periodicity 2 modulo 3 associated with the shifted frame -1 (maximal values of the function at i = 2, 5, 8 etc). Furthermore, the classification of i-motifs according to the type of periodicity demonstrates a strong coherence relation between the 64 i-motifs, which is, in addition, common to the three gene populations, as the same i-motifs in the three gene populations have the same periodicities. The three periodicities 0, 1 and 2 modulo 3 can be simulated by an evolutionary model at two successive processes. The simulated genes are generated by a process of gene construction, with a stochastic automaton followed by a process of gene evolution with random insertions and deletions of trinucleotides simulating RNA editing. For almost all i-motifs, the autocorrelation functions in these simulated genes are strongly correlated with those in protein coding genes, for both the type and the probability level of periodicities. This paper describes the process of ribosomal frameshifting leading to the shifted periodicities, which may reveal overlapping genes or concatenated genes from different frames. It also presents the evolutionary aspects of the shifted periodicities. The shifted periodicities cannot be associated with the RNY model (Eigen & Schuster, 1978, Naturwissenschaften 65, 341-369) or the RRY model (Crick et al., 1976, Origins of Life 7, 389-397), but are compatible with the oligonucleotide mixing model (Arquès & Michel, 1990, Bull. math. Biol. 52, 741-772). Finally, a variant of the primitive translation model of Crick et al. (1976) is proposed to explain the shifted periodicities.
Animals↗