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Patients with severe COVID-19 exhibit a cytokine storm characterized by greatly elevated levels of cytokines during worsening disease. Despite this, the interferon (IFN) response is delayed, contributing to disease progression. Here, we report that SARS-CoV-2 generates excessive amounts of small viral RNAs (svRNAs) encoding exact 5′ ends of positive-sense genes in human cells, whereas significantly fewer similar svRNAs are produced by endemic human coronaviruses (OC43 and 229E). SARS-CoV-2 5′ end svRNAs are RIG-I agonists associated with IFN-beta expression in later stages of infection. The first 60-nt ends bearing duplex structures and 5′-triphosphates are responsible for immune-stimulation. The 5′ end svRNAs were also produced during infection ex vivo and in vivo. The delta variant retains the robust 5′ end svRNA production of the parental strain, whereas omicron (BA.1 and BA.2) produces little of these erroneous svRNAs. We propose that RIG-I activation by accumulated 5′ end svRNAs overcomes the initial IFN antagonistic ability of viral proteins and contributes to drive late over-exuberant IFN production leading to the development of severe COVID-19 and suggest that evolutionary modification of SARS-CoV-2 5′ end svRNA production may correlate with the reduced disease severity likely seen with omicron (BA.1 and BA.2).

Patients with severe COVID-19 exhibit a cytokine storm characterized by greatly elevated levels of cytokines during worsening disease1-4. Despite this, the interferon (IFN) response is delayed, contributing to disease progression5. Here, we report that SARS-CoV-2 generates excessive amounts of small viral RNAs (svRNAs) encoding exact 5′ ends of positive sense genes in human cells, whereas significantly fewer similar svRNAs are produced by endemic human coronaviruses (OC43 and 229E). SARS-CoV-2 5′ end svRNAs are potent RIG-I agonists associated with IFN-β expression in later stages of infection. The first 60-nt ends bearing duplex structures and 5′-triphosphates are responsible for immune-stimulation. The 5′ end svRNAs were also produced during infection in vivo. The delta variant retains the robust 5’ end svRNA production of the parental strain, whereas omicron no longer produces these erroneous svRNAs. We propose that RIG-I activation by accumulated 5′ end svRNAs overcomes the initial IFN antagonistic ability of viral proteins and drives late over-exuberant IFN production leading to the development of severe COVID-19 and suggest that evolutionary modification of SARS-CoV-2 5’ end svRNA production may correlate with the reduced disease severity likely seen with omicron.

Adiponectin is most abundantly expressed in adipose tissue and well known to play an important role in metabolic regulation. Several studies have attempted to identify the genetic determinants of metabolic syndrome (MetS), though no study has revealed a cis- or trans-single nucleotide polymorphism (SNP) that affects plasma adiponectin levels, except the adiponectin structure gene and genes encoding adiponectin-regulatory proteins. We performed a genome-wide association study in regards to plasma adiponectin concentrations in 3,310 Japanese subjects. We identified the strongest statistically associated SNP (rs4783244) with adiponectin levels (P = 3.8 × 10(-19)) in the first intron of CDH13 (T-cadherin) gene in a 30-kb haplotype block covering the promoter region to first intron. In addition, rs12051272 SNP genotypes in linkage disequilibrium with rs4783244 were found to be more significantly associated with adiponectin levels (P = 9.5×10(-20)) and specifically with the levels of high-molecular weight (HMW) adiponectin, a subtype form associated with parameters related to glucose metabolism. Our results did show more significant association with adiponectin levels than rs12444338 (in CDH13) SNP genotypes reported recently. We suggest that the phenotype-affecting haplotype tagged by rs12051272 SNP would affect the plasma adiponectin levels and that we have to take the CDH13 genotype into account before considering the functional relevance of the adiponectin level.

Aim: The autosomal recessive hypercholesterolemia (ARH) gene is located on chromosome 1p35 and encodes a 308-amino acid protein containing a phosphotyrosine-binding domain. Several researchers have identified mutations of ARH that cause autosomal recessive hypercholesterolemia; however, it remains unknown whether this gene is involved in common hypercholesterolemia.Methods and Results: We searched for polymorphisms of the ARH gene by denaturing high-performance liquid chromatography and direct sequencing. We identified 18 single nucleotide polymorphisms of the gene, including 9 novel polymorphisms, and determined 2 haplotype blocks. No association was observed between common hypercholesterolemia and any polymorphisms or haplotypes of the ARH gene; however, we newly identified a rare Thr56Met missense mutation located in the phosphotyrosine-binding domain, which is the functional domain responsible for cholesterol metabolism. Among 1,800 Japanese individuals enrolled in the Suita study, only 4 were heterozygous for Thr56Met and all had hypercholesterolemia. The total cholesterol level and low-density lipoprotein cholesterol level of diabetic patients with the Thr56Met missense mutation was 276.3±13.8mg/dL and 185.3±7.37mg/dL, respectively.Conclusions: Because the Thr56Met missense mutation occurs in an orthologously conserved functional domain and all subjects with the mutation had hypercholesterolemia resembling familiar hypercholesterolemia, it may be a cause of familial hypercholesterolemia.

Approximately 20% of aortic aneurysm and/or dissection (AAD) cases result from inherited disorders, including several systemic and syndromatic connective-tissue disorders, such as Marfan syndrome, Ehlers-Danlos syndrome, and Loeys-Dietz syndrome, which are caused by mutations in the FBN1, COL3A1, and TGFBR1 and TGFBR2 genes, respectively. Nonsyndromatic AAD also has a familial background, and mutations of the ACTA2 gene were recently shown to cause familial AAD. In the present study, we conducted sequence analyses of the ACTA2 gene in 14 unrelated Japanese patients with familial thoracic AAD (TAAD), and in 26 with sporadic and young-onset TAAD. Our results identified three mutations of ACTA2, two novel [p.G152_T205del (c.616+1G>T), p.R212Q] and one reported (p.R149C), in the 14 patients with familial TAAD, and a novel mutation (p.Y145C) of ACTA2 in the 26 sporadic and young-onset TAAD patients, each of which are considered to be causative for TAAD. Some of the clinical features of these patients were the same as previously reported, whereas others were different. These findings confirm that ACTA2 mutations are important in familial TAAD, while the first sporadic and young-onset TAAD case with an ACTA2 mutation was also identified. Hum Mutat 30:1–6, 2009. © 2009 Wiley-Liss, Inc.

11β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1), one of the isoforms of the 11β-hydroxysteroid dehydrogenase enzymes, acts as an oxo-reductase to reactivate cortisone to cortisol, plays a critical role in tissue-specific corticosteroid reactions, and is therefore a key molecule associated with the development of metabolic syndrome. We investigated whether variations in the 11β-HSD1 gene correlated with metabolic syndrome. We performed case–control study using a population-based urban Japanese cohort. Among 3005 urban residents, we examined 431 subjects diagnosed with metabolic syndrome according to the Japanese definition and 777 subjects with none of metabolic syndrome criteria as control. We genotyped three single nucleotide polymorphisms (SNPs) (+9410T>A, +17925C>T, +27447G>C) across the 11β-HSD1 gene in them and analyzed the associations of SNPs and haplotypes with metabolic syndrome. The +9410A allele showed a tendency to metabolic syndrome (OR = 1.5, 95%C.I., 1.0–2.2; P = 0.041 and Bonferroni corrected P = 0.123) without statistical significance. However, we could not find any significant association between metabolic syndrome and SNPs in the 11β-HSD1 gene. Our findings indicate that polymorphisms and haplotypes in the 11β-HSD1 gene are not significantly associated with metabolic syndrome in the Japanese population.

Summary Objectives Metabolic syndrome is defined as a cluster of risk factors for cardiovascular disease and is intimately related to insulin resistance. Resistin, a hormone secreted by adipocytes, may play an important role in communication between adiposity and insulin resistance. We investigated whether variations in the resistin gene associated with metabolic syndrome in a Japanese population. Method We analyzed five SNPs, two of which were located in the promoter region (−420C > G, −358G > A), two in intron 2 (+157C > T, +299G > A), and one in the 3′-untranslated region (3′UTR) (+1263G > C) across the resistin gene in 2968 residents from an urban Japanese cohort. The associations of SNPs and haplotypes with metabolic syndrome were analyzed. Results The GAC and CGC haplotypes (comprising −420C > G, −358G > A, and +157C > T) had opposite influences on metabolic syndrome susceptibility in men; the former was associated with an increased risk and the latter with a decreased risk. We also found that the −420G allele was significantly associated with an increased risk of metabolic syndrome and significantly correlated with high diastolic blood pressure, high HOMA-IR values, high serum triglyceride levels, low HDL-cholesterol levels and high serum levels of adiponectin. Conclusion We identified a risk-conferring SNP and haplotype of the resistin gene for metabolic syndrome in a Japanese population. Our data suggested that resistin gene is a susceptibility gene for metabolic syndrome in Japanese men.

This study targets the process that forms three-dimensional plastic film from a two-dimensional printed arbitrary pattern. When three dimensional film is formed from two dimensional, expansions and contractions occurs. In this paper, we introduce an automatic printing system that form two-dimensional film includes partial expands and contractions to observe it naturally in three-dimensions. Our key idea is to extract three-dimensional distances with photometric stereo and to map two-dimensional patterns with Multi Dimensional Scaling (MDS) methodology. The purpose of this study is to develop an automatic printing system to form three-dimension. At present, our study provided useful information with photometric stereo and MDS, however, Further study is under way to develop the printing system.

Contains fulltext : 153458.pdf (Publisher’s version ) (Open Access) BACKGROUND: Aneurysms affecting the aorta are a common condition associated with high mortality as a result of aortic dissection or rupture. Investigations of the pathogenic mechanisms involved in syndromic types of thoracic aortic aneurysms, such as Marfan and Loeys-Dietz syndromes, have revealed an important contribution of disturbed transforming growth factor (TGF)-beta signaling. OBJECTIVES: This study sought to discover a novel gene causing syndromic aortic aneurysms in order to unravel the underlying pathogenesis. METHODS: We combined genome-wide linkage analysis, exome sequencing, and candidate gene Sanger sequencing in a total of 470 index cases with thoracic aortic aneurysms. Extensive cardiological examination, including physical examination, electrocardiography, and transthoracic echocardiography was performed. In adults, imaging of the entire aorta using computed tomography or magnetic resonance imaging was done. RESULTS: Here, we report on 43 patients from 11 families with syndromic presentations of aortic aneurysms caused by TGFB3 mutations. We demonstrate that TGFB3 mutations are associated with significant cardiovascular involvement, including thoracic/abdominal aortic aneurysm and dissection, and mitral valve disease. Other systemic features overlap clinically with Loeys-Dietz, Shprintzen-Goldberg, and Marfan syndromes, including cleft palate, bifid uvula, skeletal overgrowth, cervical spine instability and clubfoot deformity. In line with previous observations in aortic wall tissues of patients with mutations in effectors of TGF-beta signaling (TGFBR1/2, SMAD3, and TGFB2), we confirm a paradoxical up-regulation of both canonical and noncanonical TGF-beta signaling in association with up-regulation of the expression of TGF-beta ligands. CONCLUSIONS: Our findings emphasize the broad clinical variability associated with TGFB3 mutations and highlight the importance of early recognition of the disease because of high cardiovascular risk.

Finding genes by the positional candidate approach requires abundant cDNAs mapped to chromosomes. To provide such important information, we computationally mapped 19032 of our mouse cDNAs to mouse chromosomes by using data from public databases. We used 2 approaches. In the first, we integrated the mapping data of cDNAs on the human genome, known gene-related data, and comparative mapping data. From this, we calculated map positions on the mouse chromosomes. For this first approach, we developed a simple and powerful criterion to choose the correct map position from candidate positions in sequence homology searches. In the second approach, we related cDNAs to expressed sequence tags (EST) previously mapped in radiation hybrid experiments. We discuss improving the mapping by combining the 2 methods.

From the time-independent current $\tcj(\bar y,\bar k)$ in the quantum self-dual Yang-Mills (SDYM) theory, we construct new group-valued quantum fields $\tilde U(\bar y,\bar k)$ and $\bar U^{-1}(\bar y,\bar k)$ which satisfy a set of exchange algebras such that fields of $\tcj(\bar y,\bar k)\sim\tilde U(\bar y,\bar k)~\partial\bar y~\tilde U^{-1}(\bar y,\bar k)$ satisfy the original time-independent current algebras. For the correlation functions of the products of the $\tilde U(\bar y,\bar k)$ and $\tilde U^{-1}(\bar y,\bar k)$ fields defined in the invariant state constructed through the current $\tcj(\bar y,\bar k)$ we can derive the Knizhnik-Zamolodchikov (K-Z) equations with an additional spatial dependence on $\bar k$. From the $\tilde U(\bar y,\bar k)$ and $\tilde U^{-1}(\bar y,\bar k)$ fields we construct the quantum-group generators --- local, global, and semi-local --- and their algebraic relations. For the correlation functions of the products of the $\tilde U$ and $\tilde U^{-1}$ fields defined in the invariant state constructed through the semi-local quantum-group generators we obtain the quantum-group difference equations. We give the explicit solution to the two point function., 15 pages, uses phyzzx

OBJECTIVE In white adipose tissue, adipocytes and adipocyte precursor cells are enmeshed in a dense network of type I collagen fibrils. The fate of this pericellular collagenous web in diet-induced obesity, however, is unknown. This study seeks to identify the genetic underpinnings of proteolytic collagen turnover and their association with obesity progression in mice and humans. RESEARCH DESIGN AND METHODS The hydrolysis and degradation of type I collagen at early stages of high-fat diet feeding was assessed in wild-type or MMP14 (MT1-MMP)-haploinsufficient mice using immunofluorescent staining and scanning electron microscopy. The impact of MMP14-dependent collagenolysis on adipose tissue function was interrogated by transcriptome profiling with cDNA microarrays. Genetic associations between MMP14 gene common variants and obesity or diabetes traits were examined in a Japanese cohort (n = 3,653). RESULTS In adult mice, type I collagen fibers were cleaved rapidly in situ during a high-fat diet challenge. By contrast, in MMP14 haploinsufficient mice, animals placed on a high-fat diet were unable to remodel fat pad collagen architecture and display blunted weight gain. Moreover, transcriptional programs linking type I collagen turnover with adipogenesis or lipogenesis were disrupted by the associated decrease in collagen turnover. Consistent with a key role played by MMP14 in regulating high-fat diet–induced metabolic programs, human MMP14 gene polymorphisms located in proximity to the enzyme's catalytic domain were closely associated with human obesity and diabetes traits. CONCLUSIONS Together, these findings demonstrate that the MMP14 gene, encoding the dominant pericellular collagenase operative in vivo, directs obesogenic collagen turnover and is linked to human obesity traits.

This paper analyzes the legal effect of Geishogi-contract in the early Meiji period, before the enforcement of Old Civil Law, with some unknown decisions of lower courts in Tokyo and Osaka.It contains, First, as for Geishogi-contract, dualistic opinions, labor contract as Geishogi was void against public policy but advance contract was valid, had been dominant during the Old Supreme Court era. In 1955, Supreme Court invalidated the long supported precedent with a unitary opinion and reversed it. This paper clarified, for the first time, that dualistic opinions (e. g., the decision of Tokyo court of appeals in 1878, the decision of Tokyo district court in 1879) had existed before the appearance of the decision of Old Supreme Court and that had been the main stream in lower courts.Second, while there had been the decision of Old Supreme Court in 1896 for Geishogi's freedom of retirement, similarly, we found that it had been admitted in lower courts (Tokyo and Osaka) before it. Furth-ermore, there were interesting decisions that had prohibited a master from forcing Geishogi to work and from taking back the returned. In the case of human traffic as an employment contract, lower courts had remedies for Geishogi's freedom of retirement with dualistic opinions.Third, we found, however, a progressive decision which made an advance contract void for the proclamation 295 in 1872. Finally, we should regard the decision, the substance of an adoption for Geigi was a masked Geishogi-contract and void for the proclamation 295, as the progressive one which was treated as a problem of public policy.

Leptin is an adipocyte-secreted hormone that regulates food intake and body weight, and that was recently reported to suppress sweet sensitivity in an animal model. We investigated the associations among sweet preference, obesity, and polymorphisms of the leptin gene (LEP) or leptin receptor gene (LEPR). A total of 3,653 residents randomly selected from among the citizens of Suita City, Osaka, Japan were enlisted as subjects, in whom we investigated sweet preference, clinical characteristics, including obesity and serum leptin level, and the polymorphisms of LEP and LEPR (G-2548A and A19G for LEP; R109K, R223Q, and rs3790439 for LEPR). We determined the associations among the parameters using logistic regression analysis, in order to consider potential confounding factors for sweet preference and/or obesity. The LEP A19G and LEPR R109K polymorphisms were associated with sweet preference, whereas the serum leptin level was not. Further, the LEPR 109KK genotype was found to be associated with obesity along with sweet preference. In conclusion, our results are the first to show associations of LEP and LEPR polymorphisms with sweet preference, and may provide useful information for diagnosis and treatment of lifestyle-related diseases.

Finding genes by the positional candidate approach requires abundant cDNAs mapped to chromosomes. To provide such important information, we computationally mapped 19032 of our mouse cDNAs to mouse chromosomes by using data from public databases. We used 2 approaches. In the first, we integrated the mapping data of cDNAs on the human genome, known gene-related data, and comparative mapping data. From this, we calculated map positions on the mouse chromosomes. For this first approach, we developed a simple and powerful criterion to choose the correct map position from candidate positions in sequence homology searches. In the second approach, we related cDNAs to expressed sequence tags (EST) previously mapped in radiation hybrid experiments. We discuss improving the mapping by combining the 2 methods.

We have used the FANTOM2 mouse cDNA set (60,770 clones), public mRNA data, and mouse genome sequence data to identify 2481 pairs of sense–antisense transcripts and 899 further pairs of nonantisense bidirectional transcription based upon genomic mapping. The analysis greatly expands the number of known examples of sense–antisense transcript and nonantisense bidirectional transcription pairs in mammals. The FANTOM2 cDNA set appears to contain substantially large numbers of noncoding transcripts suitable for antisense transcript analysis. The average proportion of loci encoding sense–antisense transcript and nonantisense bidirectional transcription pairs on autosomes was 15.1 and 5.4%, respectively. Those on the X chromosome were 6.3 and 4.2%, respectively. Sense–antisense transcript pairs, rather than nonantisense bidirectional transcription pairs, may be less prevalent on the X chromosome, possibly due to X chromosome inactivation. Sense and antisense transcripts tended to be isolated from the same libraries, where nonantisense bidirectional transcription pairs were not apparently coregulated. The existence of large numbers of natural antisense transcripts implies that the regulation of gene expression by antisense transcripts is more common that previously recognized. The viewer showing mapping patterns of sense–antisense transcript pairs and nonantisense bidirectional transcription pairs on the genome and other related statistical data is available on our Web site.

Although the sequencing of the human genome is complete, identification of encoded genes and determination of their structures remain a major challenge. In this report, we introduce a method that effectively uses full-length mouse cDNAs to complement efforts in carrying out these difficult tasks. A total of 61,227 RIKEN mouse cDNAs (21,076 full-length and 40,151 EST sequences containing certain redundancies) were aligned with the draft human sequences. We found 35,141 non-redundant genomic regions that showed a significant alignment with the mouse cDNAs. We analyzed the structures and compositional properties of the regions detected by the full-length cDNAs, including cross-species comparisons, and noted a systematic bias of GENSCAN against exons of small size and/or low GC-content. Of the cDNAs locating the 35,141 genomic regions, 3,217 did not match any sequences of the known human genes or ESTs. Among those 3,217 cDNAs, 1,141 did not show any significant similarity to any protein sequence in the GenBank non-redundant protein database and thus are candidates for novel genes.

The RIKEN Mouse Gene Encyclopaedia Project, a systematic approach to determining the full coding potential of the mouse genome, involves collection and sequencing of full-length complementary DNAs and physical mapping of the corresponding genes to the mouse genome. We organized an international functional annotation meeting (FANTOM) to annotate the first 21,076 cDNAs to be analysed in this project. Here we describe the first RIKEN clone collection, which is one of the largest described for any organism. Analysis of these cDNAs extends known gene families and identifies new ones.

We give an explicit construction of the quantum-group generators ---local, semi-local, and global --- in terms of the group-valued quantum fields $\tilde g$ and $\tilde g^{-1}$ in the Wess-Zumino-Novikov-Witten (WZNW) theory. The algebras among the generators and the fields make concrete and clear the bi-module properties of the $\tilde g$ and the $\tilde g^{-1}$ fields. We show that the correlation functions of the $\tilde g$ and $\tilde g^{-1}$ fields in the vacuum state defined through the semi-local quantum-group generator satisfy a set of quantum-group difference equations. We give the explicit solution for the two point function. A similar formulation can also be done for the quantum Self-dual Yang-Mills (SDYM) theory in four dimensions., Comment: 12 pages; uses latex; minor revisions for publication in Phys. Lett. B

Hidenori Kiyosawa, Tsugumi Kawashima, Yuki Hasegawa, Itaru Yamanaka, Katsunaga Sakai, Shinji Kondo, RIKEN GER Group and GSL Members, and Yoshihide Hayashizaki Laboratory for Genome Exploration Research Group, RIKEN Genomic Sciences, Center (GSC), RIKEN Yokohama Institute, Suehiro-cho, Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan; Division of Genomic Information Resource Exploration, Science of Biological Supramolecular Systems, Yokohama City University, Graduate School of Integrated Science, Suehiro-cho, Tsurumi-ku, Yokohama 230-0045, Japan; Genome Science Laboratory, RIKEN, Hirosawa, Wako, Saitama 351-0198, Japan

A considerable proportion of lung adenocarcinoma (LADC) cases develop through activation of oncogenes, i.e., somatic mutations in either the EGFR (10–40%) or KRAS (10–20%) genes, or fusion of the ALK gene (5%) with the EML4 or KIF5B genes, in a mutually exclusive manner. Tyrosine kinase inhibitors that target EGFR and ALK proteins are particularly effective for treating LADCs carrying EGFR mutations and ALK fusions, respectively. In this study, whole transcriptome sequencing (RNA sequencing) of 30 Japanese LADCs and three adjacent non-cancerous lung tissues was performed to identify novel chimeric fusion transcripts that could be potential targets for therapy. Analysis of more than 2 × 107 paired-end reads obtained by RNA sequencing and subsequent validation by Sanger sequencing of the reverse transcription (RT)-PCR products identified EML4-ALK fusions in two cases and a few other gene fusions in each single case. The two EML4-ALK positive LADC cases were negative for EGFR and KRAS mutations and also negative for other gene fusions. Therefore, the authenticity of ALK fusions as a driver mutation was validated. The prevalence and oncogenic property of novel gene fusions identified are being studied. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; 2011 Nov 12-16; San Francisco, CA. Philadelphia (PA): AACR; Mol Cancer Ther 2011;10(11 Suppl):Abstract nr B93.

We have constructed a quantum field theory for the self-dual Yang-Mills system in terms of the group-valued fields J^. They satisfy exchange algebras, of which the structure matrices R^ satisfy Yang-Baxter equations. We show that the fields J^ form noncommutative vector spaces of a local quantum group and their products at short distances have nontrivial critical exponents. We obtain the quantum Hamiltonian and equations of motion; identify the generators for their symmetries; and construct the affine-Lie-algebra currents, Virasoro-algebra fields, and hierarchies of linear and nonlinear systems.

We construct a canonical formulation of the self-dual Yang-Mills system formulated in the gauge-invariant group-valued {ital J} fields and derive their Hamiltonian and the quadratic algebras of the fundamental Dirac brackets. We also show that the quadratic algebras satisfy Jacobi identities and their structure matrices satisfy modified Yang-Baxter equations. From these quadratic algebras, we construct Kac-Moody-like and Virasoro-like algebras. We also discuss their related symmetries, involutive conserved quantities, and hierarchies of nonlinear and linear equations.

On montre l'equivalence entre les tenseurs impulsion-energie des modeles (super) conformes degeneres faits de fermions

On construit explicitement une representation unitaire des algebres de Virasoro avec la charge centrale c=1−6/(N+1) (N+2)

Based on the operator formalism and the Virasoro algebra, we present a simple method of constructing vertex operators describing the emission and absorption of general particles in bosonic string theories.

On etudie des relations entre des algebres super-Virasoro et des systemes super-soliton aux niveaux classique et quantique. On deduit explicitement plusieurs membres de l'ensemble infini de quantites conservees

The relationship between the conformal field theories and the soliton equations (KdV, MKdV and Sine–Gordon, etc.) at both quantum and classical levels is discussed. The quantum Sine–Gordon theory is formulated canonically. Its Hamiltonian is the vertex operator with respect to the Feigin–Fuchs–Miura form of the Virasoro algebra with central charge $c\le1$. It is found that the quantum conserved quantities of the Sine–Gordon-MKdV hierarchy are expressed as polynomial functions of the Virasoro generators. In other words, an infinite set of mutually commutative polynomial functions of the Virasoro generators is obtained. A very simple recursion formula for the quantum conserved quantities is found for the special case of $\beta^2_c=8\pi$ ($\beta_c$ is the coupling constant in Coleman’s theory of quantum Sine–Gordon).

The quantum version of an infinite set of polynomial conserved quantities of a class of soliton equations is discussed from the point of view of naive continuum field theory. By using techniques of two dimensional field theories, we show that an infinite set of quantum commuting operators can be constructed explicitly from the knowledge of its classical counterparts. The quantum operators are so constructed as to coincide with the classical ones in the ħ→0 limit (ħ; Planck's constant divided by 2π). It is expected that the explicit forms of these operators would shed some light on the structure of the infinite dimensional Lie algebras which underlie a certain class of quantum integrable systems.