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Hidekazu Suginaka

Bio: Hidekazu Suginaka is an academic researcher from Hiroshima University. The author has contributed to research in topics: Staphylococcus aureus & Peptidoglycan. The author has an hindex of 32, co-authored 93 publications receiving 3264 citations. Previous affiliations of Hidekazu Suginaka include Juntendo University & Kawasaki Medical School.


Papers
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Journal ArticleDOI
TL;DR: The Tn551 insertion site of the autolysis-deficient Staphylococcus aureus mutant RUSAL2 was cloned and used to identify the autologic gene atl in the parent strain, RN450, which is a bifunctional protein that has an amidase domain and an endo-beta-N-acetylglucosaminidase domain.
Abstract: The Tn551 insertion site of the autolysis-deficient Staphylococcus aureus mutant RUSAL2 was cloned and used to identify the autolysis gene atl in the parent strain, RN450. The open reading frame for atl was 3768 bp in length, encoding a deduced protein of 1256 amino acids and molecular size of 137,381 Da. The atl gene product is a bifunctional protein that has an amidase domain and an endo-beta-N-acetylglucosaminidase domain which must undergo proteolytic processing to generate the two extracellular lytic enzymes found in the culture broth of S. aureus.

316 citations

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TL;DR: The effects of hydrophobicities of substrate surfaces on microbial adherence were examined by using Candida albicans and Candida tropicalis and 21 denture base resin materials and the higher adherence tendency was accompanied by a lower value for the free energy change in both species.
Abstract: The effects of hydrophobicities of substrate surfaces on microbial adherence were examined by using Candida albicans and Candida tropicalis and 21 denture base resin materials. With increasing surface free energy of resin plates, increasing adherence of C. albicans and decreasing adherence of C. tropicalis were observed. The surface free energy of C. albicans is higher than that of all resin material surfaces, and C. tropicalis has surface free energy lower than that of all materials used. In calculation of the changes of free energy accompanying the adherence, the higher adherence tendency was accompanied by a lower value for the free energy change in both species. From a different standpoint, the closer the surface free energy of the substrate surface and the microorganism, the higher was the probability of adherence.

251 citations

Journal ArticleDOI
TL;DR: It is suggested that the CDT is responsible for the cytotoxic activity present in the culture supernatant and cell homogenate fractions of A. actinomycetemcomitans Y4 and may play a role in the pathogenesis of periodontal diseases.
Abstract: Actinobacillus actinomycetemcomitans has been shown to produce a soluble cytotoxic factor(s) distinct from leukotoxin. We have identified in A. actinomycetemcomitans Y4 a cluster of genes encoding a cytolethal distending toxin (CDT). This new member of the CDT family is similar to the CDT produced by Haemophilus ducreyi. The CDT from A. actinomycetemcomitans was produced in Escherichia coli and was able to induce cell distension, growth arrest in G2/M phase, nucleus swelling, and chromatin fragmentation in HeLa cells. The three proteins, CDTA, -B and -C, encoded by the cdt locus were all required for toxin activity. Antiserum raised against recombinant CDTC completely inhibited the cytotoxic activity of culture supernatant and cell homogenate fractions of A. actinomycetemcomitans Y4. These results strongly suggest that the CDT is responsible for the cytotoxic activity present in the culture supernatant and cell homogenate fractions of A. actinomycetemcomitans Y4. This CDT is a new putative virulence factor of A. actinomycetemcomitans and may play a role in the pathogenesis of periodontal diseases.

216 citations

Journal ArticleDOI
TL;DR: It is demonstrated that atl gene products are cell associated (unpublished data), and the formation of a ring structure of atL gene products may be required for efficient partitioning of daughter cells after cell division.
Abstract: atl is a newly discovered autolysin gene in Staphylococcus aureus. The gene product, ATL, is a unique, bifunctional protein that has an amidase domain and a glucosaminidase domain. It undergoes proteolytic processing to generate two extracellular peptidoglycan hydrolases, a 59-kDa endo-beta-N-acetylglucosaminidase and a 62-kDa N-acetylmuramyl-L-alanine amidase. It has been suggested that these enzymes are involved in the separation of daughter cells after cell division. We recently demonstrated that atl gene products are cell associated (unpublished data). The cell surface localization of the atl gene products was investigated by immunoelectron microscopy using anti-62-kDa N-acetylmuramyl-L-alanine amidase or anti-51-kDa endo-beta-N-acetylglucosaminidase immunoglobulin G. Protein A-gold particles reacting with the antigen-antibody complex were found to form a ring structure on the cell surface at the septal region for the next cell division site. Electron microscopic examination of an ultrathin section of the preembedded sample revealed preferential distribution of the gold particles at the presumptive sites for cell separation where the new septa had not been completed. The distribution of the gold particles on the surface of protoplast cells and the association of the gold particles with fibrous materials extending from the cells suggested that some atl gene products were associated with a cellular component extending from the cell membrane, such as lipoteichoic acid. The formation of a ring structure of atl gene products may be required for efficient partitioning of daughter cells after cell division.

204 citations

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TL;DR: Among the 4 fluoroquinolones, LVFX and SPFX demonstrated excellent permeation with penetration rates that reached 100% from day 0 to 5, while OFLX and CPFX showed almost the same permeation as IPM.
Abstract: In this study, we evaluated the permeation of piperacillin (PIPC), imipenem (IPM), amikacin (AKM), gentamicin (GM), ofloxacin (OFLX), levofloxacin (LVFX), ciprofloxacin (CPFX) and sparfloxacin (SPFX)

187 citations


Cited by
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Journal ArticleDOI
TL;DR: The features of biofilm infections are summarized, the emerging mechanisms of resistance are reviewed, and potential therapies are discussed.

4,116 citations

Journal ArticleDOI
TL;DR: In this review, functions of small G proteins and their modes of activation and action are described.
Abstract: Small GTP-binding proteins (G proteins) exist in eukaryotes from yeast to human and constitute a superfamily consisting of more than 100 members. This superfamily is structurally classified into at least five families: the Ras, Rho, Rab, Sar1/Arf, and Ran families. They regulate a wide variety of cell functions as biological timers (biotimers) that initiate and terminate specific cell functions and determine the periods of time for the continuation of the specific cell functions. They furthermore play key roles in not only temporal but also spatial determination of specific cell functions. The Ras family regulates gene expression, the Rho family regulates cytoskeletal reorganization and gene expression, the Rab and Sar1/Arf families regulate vesicle trafficking, and the Ran family regulates nucleocytoplasmic transport and microtubule organization. Many upstream regulators and downstream effectors of small G proteins have been isolated, and their modes of activation and action have gradually been elucidated. Cascades and cross-talks of small G proteins have also been clarified. In this review, functions of small G proteins and their modes of activation and action are described.

2,520 citations

Journal ArticleDOI
TL;DR: The mechanisms that underlie biofilm resistance to antimicrobial chemotherapy will be examined, with particular attention being given to potential avenues for the effective treatment of biofilms.
Abstract: According to a public announcement by the US National Institutes of Health , “Biofilms are medically important, accounting for over 80% of microbial infections in the body”. Yet bacterial biofilms remain poorly understood and strategies for their control remain underdeveloped. Standard antimicrobial treatments typically fail to eradicate biofilms, which can result in chronic infection and the need for surgical removal of afflicted areas. The need to create effective therapies to counter biofilm infections presents one of the most pressing challenges in anti-bacterial drug development. In this article, the mechanisms that underlie biofilm resistance to antimicrobial chemotherapy will be examined, with particular attention being given to potential avenues for the effective treatment of biofilms.

2,302 citations

Journal ArticleDOI
Kim Lewis1
TL;DR: The nature of bacterial biofilm resistance to antimicrobials is the subject of the present minireview and describes an increased resistance of cells to killing.
Abstract: A biofilm is a population of cells growing on a surface and enclosed in an exopolysaccharide matrix. Biofilms are notoriously difficult to eradicate and are a source of many recalcitrant infections. The nature of bacterial biofilm resistance to antimicrobials is the subject of the present minireview. Pathogenic yeast such as Candida albicans also form recalcitrant biofilms, and this topic has recently been reviewed (5). Resistance is an ability of a microorganism to grow in the presence of an elevated level of an antimicrobial. In short, a strain for which the MIC is increased is resistant. By this conventional criterion, biofilm cells do not necessarily show increased resistance. With some exceptions, biofilm cells do not grow better than planktonic cells in the presence of a broad range of antimicrobials. This is evident from examination of susceptibility data in the biofilm literature (33). However, in most biofilm susceptibility studies, only survival of cells in a preformed biofilm rather than the ability of a biofilm to grow is recorded. Accordingly, the reported “resistance” describes an increased resistance of cells to killing. This is indeed what biofilms are good at: they are not easily eradicated by cidal antimicrobials. The ability of antimicrobials to inhibit biofilm growth indicates that they are able to diffuse through the biofilm and act normally against their targets. Why, then, do biofilm cells not die? This is the crux of the problem and the riddle that needs to be solved.

1,830 citations

Journal ArticleDOI
TL;DR: Analysis of CA-MRSA isolates from the United States, France, Switzerland, Australia, New Zealand, and Western Samoa indicated distinct genetic backgrounds associated with each geographic origin, although predominantly restricted to the agr3 background.
Abstract: Infections caused by community-acquired (CA)-methicillin-resistant Staphylococcus aureus (MRSA) have been reported worldwide. We assessed whether any common genetic markers existed among 117 CA-MRSA isolates from the United States, France, Switzerland, Australia, New Zealand, and Western Samoa by performing polymerase chain reaction for 24 virulence factors and the methicillinresistance determinant. The genetic background of the strain was analyzed by pulsed-field gel electrophoresis (PFGE) and multi-locus sequence typing (MLST). The CAMRSA strains shared a type IV SCCmec cassette and the Panton-Valentine leukocidin locus, whereas the distribution of the other toxin genes was quite specific to the strains from each continent. PFGE and MLST analysis indicated distinct genetic backgrounds associated with each geographic origin, although predominantly restricted to the agr3 background. Within each continent, the genetic background of CA-MRSA strains did not correspond to that of the hospital-acquired MRSA.

1,790 citations