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Coronaviruses (CoV) emerge suddenly from animal reservoirs to cause novel diseases in new hosts. Discovered in 2012, the Middle East respiratory syndrome coronavirus (MERS-CoV) is endemic in camels in the Middle East and is continually causing local outbreaks and epidemics. While all three newly emerging human CoVs from the past 20 years (SARS-CoV, SARS-CoV-2, and MERS-CoV) cause respiratory disease, each CoV has unique host interactions that drive differential pathogeneses.

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Alien toxic toads suppress individual growth and phenotypic development of native predatory salamanders.

Oecologia

January 2025

Tomakomai Experimental Forest, Field Science Center for Northern Biosphere, Hokkaido University, Takaoka, Tomakomai, Hokkaido, 053-0035, Japan.

Alien species can influence populations of native species through individual-level effects such as predation, competition, and poisoning. For alien species that possess strong defensive chemicals, poisoning is one of the most powerful mechanisms of individual-level effects on native biota. Although toxic alien species could potentially negatively affect survival (lethal effects) or life history traits (sub-lethal effects) of native predators via poisoning, previous studies have mainly focused on acute lethal effects.

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In modern agriculture, control of insect pests is achieved by using insecticides that can also have lethal and sublethal effects on beneficial non-target organisms. Here, we investigate acute toxicity and sublethal effects of four insecticides on the males' sex pheromone response and the female host finding ability of the Drosophila parasitoid Leptopilina heterotoma. The nicotinic acetylcholine receptor antagonists acetamiprid, flupyradifurone and sulfoxaflor, as well as the acetylcholinesterase inhibitor dimethoate were applied topically as acetone solutions.

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Exposure to influenza A virus (IAV), respiratory syncytial virus (RSV), and human metapneumovirus (hMPV) is well-known to increase the risk of pneumonia in humans. Type I interferon (IFN-I) is a hallmark response to acute viral infections, and alveolar macrophages (AMs) constitute the first line of airway defense against opportunistic bacteria. Our study reveals that virus-induced IFN-I receptor (IFNAR1) signaling directly impairs AM-dependent antibacterial protection.

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