Can Photons Pass through Primary Coatings Used to Treat Cutaneous Wounds?

OBJECTIVE: To determine the transmittance spectrum of primary dressings commonly used in the treatment of cutaneous wounds to verify if there is a real need to remove them during photobiomodulation. METHODS: Spectroscopic analysis was performed on 17 dressings using a spectrophotometer (USB 2000+; OceanOptics, Delray Beach, Florida). A piece of each dressing was inserted into a quartz cuvette; the reflection from the slide walls was corrected for using a 0.9% saline solution to completely fill the cuvette (baseline). The transmittance of each dressing was measured between 350 and 950 nm, and a transmittance table was created based on the main wavelengths used in photobiomodulation. RESULTS: Six dressings (Supriderme, Membracel, Cuticell Contact, UrgoTul, Tegaderm, and Opsite Flexigrid) have a transmittance greater than 50% in most of the spectral range and therefore may remain on wounds during irradiation. CONCLUSIONS: It may not always be necessary to remove a primary dressing when lasers or LED lights are used to treat wounds. It is the authors' hope that the results of this article will increase the effectiveness of both photobiomodulation and primary dressings and reduce patient discomfort as well as the cost of primary dressings via a reduction in unnecessary dressing changes.

When and how NK cell-induced programmed cell death benefits immunological protection against intracellular pathogen infection.

NK cells are innate lymphoid cells that exert a key role in immune surveillance through the recognition and elimination of transformed cells and viral, bacterial, and protozoan pathogen-infected cells without prior sensitization. Elucidating when and how NK cell-induced intracellular microbial cell death functions in the resolution of infection and host inflammation has been an important topic of investigation. NK cell activation requires the engagement of specific activating, co-stimulatory, and inhibitory receptors which control positively and negatively their differentiation, memory, and exhaustion. NK cells secrete diverse cytokines, including IFN-γ, TNF-α/ß, CD95/FasL, and TRAIL, as well as cytoplasmic cytotoxic granules containing perforin, granulysin, and granzymes A and B. Paradoxically, NK cells also kill other immune cells like macrophages, dendritic cells, and hyper-activated T cells, thus turning off self-immune reactions. Here we first provide an overview of NK cell biology, and then we describe and discuss the life-death signals that connect the microbial pathogen sensors to the inflammasomes and finally to cell death signaling pathways. We focus on caspase-mediated cell death by apoptosis and pro-inflammatory and non-caspase-mediated cell death by necroptosis, as well as inflammasome- and caspase-mediated pyroptosis.

Effects of Cetuximab and Erlotinib on the behaviour of cancer stem cells in head and neck squamous cell carcinoma.

The therapeutic responses of many solid tumours to chemo- and radio-therapies are far from fully effective but therapies targeting malignancy-related cellular changes show promise for further control. In head and neck squamous cell carcinoma, the epidermal growth factor receptor (EGFR) is commonly overexpressed and investigation of agents that block this receptor indicate a limited response when used alone but an ability to enhance the actions of other drugs. The hierarchical stem cell patterns present in tumours generate cellular heterogeneity and this is further complicated by cancer stem cells (CSC) shifting between epithelial (Epi-CSC) and mesenchymal (EMT-CSC) states. To clarify how such heterogeneity influences responses to EGFR blocking, we examined the effects of Cetuximab and Erlotinib on the cell sub-populations in HNSCC cell lines. These agents reduced cell proliferation for all subpopulations but induced little cell death. They did however induce large shifts of cells between the EMT-CSC, Epi-CSC and differentiating cell compartments. Loss of EMT-CSCs reduced cell motility and is expected to reduce invasion and metastasis. EGFR blocking also induced shifts of Epi-CSCs into the differentiating cell compartment which typically has greater sensitivity to chemo/radiation, an effect expected to enhance the overall response of tumour cell populations to adjunctive therapies.