If we are in the book of Sarah now would this count?
EN A STAR I AM OS
beeste
plural of bees
beasting
present participle of beast
bee sting
noun: bee sting; plural noun: bee stings
a wound from the sting of a bee.
"those who are allergic to bee stings may have an adverse reaction to pollen"
hornet
definite singular of horn
horn m (nominative plural hornas)
horn
(horn-shaped) gable
An acoustic horn or waveguide is a tapered sound guide designed to provide an acoustic impedance match between a sound source and free air. This has the effect of maximizing the efficiency with which sound waves from the particular source are transferred to the air.
Hiker-Kayaker-Bicyclist-Paddleboarder (⊙﹏⊙✿) life➭the way I see it, posted here ☯︎_0️⃣social.creditz
how'd you get a video of my neighbor's ass while she's walking to her car ? 😜
Hiker-Kayaker-Bicyclist-Paddleboarder (⊙﹏⊙✿) life➭the way I see it, posted here ☯︎_0️⃣social.creditz
tumour
/ˈtjuːmə/
noun: tumor
a swelling of a part of the body, generally without inflammation, caused by an abnormal growth of tissue, whether benign or malignant.
cancerous growth
malignant growth
cancer
malignancy
lump
growth
swelling
carcinoma
sarcoma
melanoma
lymphoma
myeloma
neoplasm
metastasis
neurofibroma
teratoma
fibroadenoma
meningioma
Oxidative stress induced by engineered NP is due to acellular factors such as particle surface, size, composition, and presence of metals, while cellular responses such as mitochondrial respiration, NP-cell interaction, and immune cell activation are responsible for ROS-mediated damage. NP-induced oxidative stress responses are torch bearers for further pathophysiological effects including genotoxicity, inflammation, and fibrosis as demonstrated by activation of associated cell signaling pathways. Since oxidative stress is a key determinant of NP-induced injury, it is necessary to characterize the ROS response resulting from NP. Through physicochemical characterization and understanding of the multiple signaling cascades activated by NP-induced ROS, a systemic toxicity screen with oxidative stress as a predictive model for NP-induced injury can be developed.
The toxic potential of NPs is dependent on their size and shape, which determined their propensity to induce the generation of reactive oxygen species (ROS) [20, 21]. The excess generation ROS may induce an array of physiopathologic outcomes, including genotoxicity, apoptosis, necrosis, inflammation, fibrosis, metaplasia, hypertrophy, and carcinogenesis [18, 22, 23].
The toxicity of NPs has also been shown to enhance the expression of pro-inflammatory cytokines and activate inflammatory cells, such as macrophages, which further increase the generation of ROS [23, 24]. The increased generation of ROS following exposure to NPs has been also shown to induce the modulation of cellular functions, with fatal results in some cases [17, 23, 25]. In this review, we discuss the main mechanisms underlying the ROS bursts induced by NPs, analyze the primary reasons for the cytotoxicity of NPs, and summarize the potential pathogenic effects of NPs. Our present review provides overwhelming evidence that the over-production of ROS is the major cause of the biotoxicity of NPs. Therefore, novel research should aim to reduce the cytotoxicity of NPs by designing NPs which induce low ROS production.
