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fasciitis/protease

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مقالاتالتجارب السريريةبراءات الاختراع
الصفحة 1 من عند 54 النتائج

Structure of ScpC, a virulence protease from Streptococcus pyogenes, reveals the functional domains and maturation mechanism.

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Group A Streptococcus (GAS; Streptococcus pyogenes) causes a wide range of infections, including pharyngitis, impetigo, and necrotizing fasciitis, and results in over half a million deaths annually. GAS ScpC (SpyCEP), a 180-kDa surface-exposed, subtilisin-like serine protease, acts as an essential

Nodular fasciitis involving the palm.

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Nodular fasciitis (NF) is a self-limiting fibrous neoplasm that can be mistaken for a soft tissue sarcoma. It is characterised by rapid growth, slight pain and local tenderness. Although it is frequently found in the forearm, a lesion distal to the wrist is quite rare. We present two unusual cases

Nodular fasciitis of the temporomandibular joint: a case report.

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Nodular fasciitis is a relatively rare benign lesion of the soft tissue, which often presents in the fascia or deep subcutaneous tissues. It most commonly presents in the upper extremities and trunk and the head and neck region, particularly in younger patients. Its pathogenesis is poorly understood

Decreased necrotizing fasciitis capacity caused by a single nucleotide mutation that alters a multiple gene virulence axis.

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Single-nucleotide changes are the most common cause of natural genetic variation among members of the same species, but there is remarkably little information bearing on how they alter bacterial virulence. We recently discovered a single-nucleotide mutation in the group A Streptococcus genome that

Chemokine-cleaving Streptococcus pyogenes protease SpyCEP is necessary and sufficient for bacterial dissemination within soft tissues and the respiratory tract.

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SpyCEP is a Streptococcus pyogenes protease that cleaves CXCL8/IL-8 and its activity is associated with human invasive disease severity. We investigated the role of SpyCEP in S. pyogenes necrotizing fasciitis and respiratory tract infection in mice using isogenic strains differing only in SpyCEP

Polymorphisms in regulator of protease B (RopB) alter disease phenotype and strain virulence of serotype M3 group A Streptococcus.

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Whole-genome sequencing of serotype M3 group A streptococci (GAS) from oropharyngeal and invasive infections in Ontario recently showed that the gene encoding regulator of protease B (RopB) is highly polymorphic in this population. To test the hypothesis that ropB is under diversifying selective

Streptococcus pyogenes transcriptome changes in inflammatory environment of necrotizing fasciitis.

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Streptococcus pyogenes is a major cause of necrotizing fasciitis, a life-threatening subcutaneous soft-tissue infection. At the host infection site, the local environment and interactions between the host and bacteria have effects on bacterial gene-expression profiles, while the

From transcription to activation: how group A streptococcus, the flesh-eating pathogen, regulates SpeB cysteine protease production.

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Streptococcal pyrogenic exotoxin B (SpeB) is a protease secreted by group A streptococci and known to degrade a wide range of host and GAS proteins in vitro. Although the role of SpeB in GAS infection is debated, recent evidence has conclusively demonstrated that SpeB is critical for the

Crystal structure of the zymogen form of the group A Streptococcus virulence factor SpeB: an integrin-binding cysteine protease.

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Pathogenic bacteria secrete protein toxins that weaken or disable their host, and thereby act as virulence factors. We have determined the crystal structure of streptococcal pyrogenic exotoxin B (SpeB), a cysteine protease that is a major virulence factor of the human pathogen Streptococcus pyogenes

Vaccine based on a ubiquitous cysteinyl protease and streptococcal pyrogenic exotoxin A protects against Streptococcus pyogenes sepsis and toxic shock.

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BACKGROUND The gram-positive bacterium Streptococcus pyogenes is a common pathogen of humans that causes invasive infections, toxic-shock syndrome, rheumatic fever, necrotizing fasciitis and other diseases. Detection of antibiotic resistance in clinical isolates has renewed interest in development

Necrotizing fasciitis and myositis caused by group A streptococci. Epidemiology, diagnosis, and treatment of "flesh-eating bacteria".

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Despite the absence of conclusive proof, the incidence of necrotizing fasciitis and myositis due to GAS may be increasing, possibly related to shifts in the proportion of GAS isolates of M-Types 1 and 3. These M-types (or the production of exotoxins and proteases associated with them) may lead to

Exploring the pathogenesis of necrotizing fasciitis due to Streptococcus pneumoniae.

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Monobacterial necrotizing fasciitis is a rare form of soft tissue infection usually caused by the group A beta-hemolytic Streptococcus. Soft tissue infection is an uncommon clinical manifestation of invasive disease due to Streptococcus pneumoniae. We describe 3 cases of pneumococcal necrotizing

USP6 Gene Rearrangement by FISH Analysis in Cranial Fasciitis: A Report of Three Cases.

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Cranial fasciitis (CF) is an uncommon benign myofibroblastic proliferation involving the soft and hard tissues of the cranium. It typically occurs in the pediatric population with a male predilection (male-to-female ratio 1.5:1). The clinical presentation is usually a rapidly expanding, painless

Relatedness of Streptococcus canis from canine streptococcal toxic shock syndrome and necrotizing fasciitis.

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The emergence of streptococcal toxic shock syndrome (STSS) and necrotizing fasciitis (NF) in dogs caused by Streptococcus canis has been reported by our laboratory. Since clonal expansion is thought to be partially responsible for the spread of invasive strains of Streptococcus pyogenes in humans,

The majority of 9,729 group A streptococcus strains causing disease secrete SpeB cysteine protease: pathogenesis implications.

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Group A streptococcus (GAS), the causative agent of pharyngitis and necrotizing fasciitis, secretes the potent cysteine protease SpeB. Several lines of evidence suggest that SpeB is an important virulence factor. SpeB is expressed in human infections, protects mice from lethal challenge when used as
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