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1 d can contribute to the host response during bone infection.
2 osomes are better than 99mTc-MDP for imaging bone infection.
3 is is a mostly posttraumatic, Staphylococcal bone infection.
4 of bacterial pathogens by osteoblasts during bone infections.
5 10 may recruit T lymphocytes to the sites of bone infections.
6 o the bone destruction seen in gram-negative bone infections.
7 g pathogens in implant-associated and native bone infections.
8 usculoskeletal (MSK) soft tissue, joint, and bone infections.
9 lococcus aureus, the most common pathogen in bone infections, adapts to multiple environments to surv
10 osteomyelitis, characterized by intractable bone infection and sequestrum formation, and can result
11 be how the host fails to eradicate bacterial bone infections, and how this new information may lead t
14 fever, lymphadenopathies, and an absence of bone infection being the differentiating elements from p
15 library of 17 candidate antibiotics against bone infection by wild-type and mutated bacterial target
16 They were responsible for soft-tissue and bone infections, catheter-related infections, and possib
18 atients with chronic skin and soft tissue or bone infections, especially in the lower extremities.
23 d infectious lymphadenitis, and of joint and bone infections including septic arthritis and osteomyel
24 idic acid (FA) has been used for decades for bone infection, including prosthetic joint infection (PJ
25 iterature, suggest mammalian descriptors for bone infection may be applicable to non-avian dinosaurs.
27 In the 2 patients with successfully treated bone infection, multiphase (99m)Tc-hydroxyethylene dipho
28 y enrolled patients with confirmed S. aureus bone infection (n = 3) or without orthopedic infection (
31 logenetic disease bracket the oldest case of bone infection (osteomyelitis) was identified in the man
32 iodontists surgically treat advanced gum and bone infection problems" was considered the most importa
34 umping factor A (clfA) showed a reduction in bone infection severity that eliminated the effect of ob
35 directly regulate inflammatory osteolysis in bone infection, suggesting that MYD88 and downstream RAN