[Publication of biological samples collections catalogues by tumor banks].

Biobanks in general, and specifically tumour banks, are considered as essential tools for the development of translational and clinical research in biology and oncology. Biobank tasks include the collection and preservation of biological samples, and their association with information that will be essential for further scientific use ("annotations" that allow for the "qualification" of biological samples in biological resource). A collection is made of a series of biological resource that are representative of a homogeneous group of individuals or patients that are defined on the basis of clinical or biological information.

RNA extracted from blood samples with a rapid automated procedure is fit for molecular diagnosis or minimal residual disease monitoring in patients with a variety of malignant blood disorders.

Scientific studies in oncology, cancer diagnosis, and monitoring tumor response to therapeutics currently rely on a growing number of clinico-pathological information. These often include molecular analyses. The quality of these analyses depends on both pre-analytical and analytical information and often includes the extraction of DNA and/or RNA from human tissues and cells.

Preeclampsia: impaired inflammatory response mediated by Toll-like receptors.

Monocytes may be activated in preeclampsia (PE). Toll-like receptor (TLR)-4 and TLR-2 are involved in inflammatory responses of monocytes. The objective of this study was to evaluate the production of tumor necrosis factor (TNF), an inflammatory cytokine, and interleukin (IL)-10, an immunoregulatory cytokine, by monocytes from PE patients stimulated with TLR ligands.

The two faces of interleukin 10 in human infectious diseases.

Resolution of infections depends on the host's ability to mount a protective immune response. However, an exacerbated response to infections may result in deleterious lesions. Consequently, immunoregulatory mechanisms are needed to control immune response and prevent infection-associated lesions.

Role for the CD28 molecule in the control of Coxiella burnetii infection.

Q fever is an infectious disease caused by Coxiella burnetii, an obligate intracellular bacterium that replicates in macrophages. As cell-mediated immune response to microbial pathogens requires signals mediated by T-cell receptors and costimulatory molecules such as CD28, we wondered if CD28 is involved in protection against C. burnetii infection.

TLR2 is necessary to inflammatory response in Coxiella burnetii infection.

The resolution of Q fever, a zoonosis caused by Coxiella burnetii, depends on efficient innate and adaptive immune responses. Such responses are influenced by Toll-like receptors (TLRs). TLR4 is involved only in part in immune responses against C.

Link between impaired maturation of phagosomes and defective Coxiella burnetii killing in patients with chronic Q fever.

Q fever is caused by Coxiella burnetii, a bacterium that survives in monocytes/macrophages by resisting their natural microbicidal activity. Because the link between bacterial killing and phagosome maturation has yet to be demonstrated, we evaluated responses in monocytes from both immunologically naive control subjects and patients with various manifestations of Q fever. Monocytes from patients with chronic Q fever in evolution, who do not control the infection, exhibited defective phagosome maturation and impaired C.

Lipopolysaccharide from Coxiella burnetii is involved in bacterial phagocytosis, filamentous actin reorganization, and inflammatory responses through Toll-like receptor 4.

The role of Toll-like receptors (TLRs) in the recognition of extracellular and facultative intracellular bacteria by the innate immune system has been extensively studied, but their role in the recognition of obligate intracellular organisms remains unknown. Coxiella burnetii, the agent of Q fever, is an obligate intracellular bacterium that specifically inhabits monocytes/macrophages. We showed in this study that C.

Effect of sex on Coxiella burnetii infection: protective role of 17beta-estradiol.

Q fever is a zoonosis caused by Coxiella burnetii and recently has been recognized as a potential agent of bioterrorism. In Q fever, men are symptomatic more often than women, despite equal seroprevalence. We hypothesized that sex hormones play a role in the pathogenesis of C.

Relationship of relapsing hip prosthesis infection by Staphylococcus aureus with gamma interferon deficiency.

Infections complicate 0.5 to 1% of surgeries for total hip prostheses. Staphylococcus species are the most common etiological agents.

Dysregulation of cytokines in acute Q fever: role of interleukin-10 and tumor necrosis factor in chronic evolution of Q fever.

Q fever manifests as primary infection or acute Q fever and may become chronic in patients with underlying valvulopathy. Because Coxiella burnetii infection depends on host response, we measured tumor necrosis factor (TNF), interleukin (IL)-6, IL-12, and IL-10 in patients with different clinical presentations of acute Q fever. Compared with control subjects, patients with uncomplicated acute Q fever exhibited increased release of the 4 cytokines.