Epidemiological Evidence of Lesser Role of Thermostable Direct Hemolysin (TDH)–Related Hemolysin (TRH) Than TDH onVibrio parahaemolyticusPathogenicity

2015 ◽  
Vol 12 (2) ◽  
pp. 131-138 ◽  
Author(s):  
Shioko Saito ◽  
Yoshito Iwade ◽  
Eisuke Tokuoka ◽  
Tomohiro Nishio ◽  
Yoshimitsu Otomo ◽  
...  
Keyword(s):  
Epidemiological Evidence ◽  
Thermostable Direct Hemolysin

scholarly journals Are Animals a Neglected Transmission Route of SARS-CoV-2?

Pathogens ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 480 ◽  
Author(s):  
Marta Hernández ◽  
David Abad ◽  
José María Eiros ◽  
David Rodríguez-Lázaro
Keyword(s):  
Close Contact ◽  
Companion Animals ◽  
Epidemiological Surveillance ◽  
Epidemiological Evidence ◽  
Exotic Animals ◽  
Animal Management ◽  
Animal Infection ◽  
Containment Measures ◽  
Exotic Animal

Little information on the SARS-CoV-2 virus in animals is available to date. Whereas no one husbandry animal case has been reported to date, which would have significant implications in food safety, companion animals play a role in COVID-19 epidemiology that opens up new questions. There is evidence that SARS-CoV-2 can infect felines, dogs and minks, and there is evidence of human-to-animal infection. Likewise, the S protein nucleotide sequence of the SARS-CoV-2 virus isolated in domestic animals and humans is identical, and the replication of the SARS-CoV-2 in cats is efficient. Besides, the epidemiological evidence for this current pandemic indicates that the spillover to humans was associated with close contact between man and exotic animals, very probably in Chinese wet markets, thus there is a growing general consensus that the exotic animal markets, should be strictly regulated. The examination of these findings and the particular role of animals in COVID-19 should be carefully analyzed in order to establish preparation and containment measures. Animal management and epidemiological surveillance must be also considered for COVID-19 control, and it can open up new questions regarding COVID-19 epidemiology and the role that animals play in it.

scholarly journals Trimethylamine N-Oxide in Relation to Cardiometabolic Health—Cause or Effect?

Nutrients ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1330 ◽  
Author(s):  
Christopher Papandreou ◽  
Margret Moré ◽  
Aouatef Bellamine
Keyword(s):  
Observational Studies ◽  
Animal Studies ◽  
Disease Model ◽  
Fish Intake ◽  
Model Systems ◽  
Cardiometabolic Health ◽  
Epidemiological Evidence ◽  
Cardiometabolic Diseases ◽  
Beneficial Effects

Trimethylamine-N-oxide (TMAO) is generated in a microbial-mammalian co-metabolic pathway mainly from the digestion of meat-containing food and dietary quaternary amines such as phosphatidylcholine, choline, betaine, or L-carnitine. Fish intake provides a direct significant source of TMAO. Human observational studies previously reported a positive relationship between plasma TMAO concentrations and cardiometabolic diseases. Discrepancies and inconsistencies of recent investigations and previous studies questioned the role of TMAO in these diseases. Several animal studies reported neutral or even beneficial effects of TMAO or its precursors in cardiovascular disease model systems, supporting the clinically proven beneficial effects of its precursor, L-carnitine, or a sea-food rich diet (naturally containing TMAO) on cardiometabolic health. In this review, we summarize recent preclinical and epidemiological evidence on the effects of TMAO, in order to shed some light on the role of TMAO in cardiometabolic diseases, particularly as related to the microbiome.

scholarly journals Lifestyle mediates the role of nutrient-sensing pathways in cognitive aging: cellular and epidemiological evidence

2020 ◽  
Vol 3 (1) ◽  
Author(s):  
Chiara de Lucia ◽  
Tytus Murphy ◽  
Claire J. Steves ◽  
Richard J. B. Dobson ◽  
Petroula Proitsi ◽  
...  
Keyword(s):  
Cognitive Aging ◽  
Nutrient Sensing ◽  
Epidemiological Evidence

scholarly journals Association of Vibrio parahaemolyticus Thermostable Direct Hemolysin with Lipid Rafts Is Essential for Cytotoxicity but Not Hemolytic Activity

2009 ◽  
Vol 78 (2) ◽  
pp. 603-610 ◽  
Author(s):  
Shigeaki Matsuda ◽  
Toshio Kodama ◽  
Natsumi Okada ◽  
Kanna Okayama ◽  
Takeshi Honda ◽  
...  
Keyword(s):  
Lipid Rafts ◽  
Hemolytic Activity ◽  
Vibrio Parahaemolyticus ◽  
Cultured Cells ◽  
Direct Interaction ◽  
Caveolin 1 ◽  
Marker Proteins ◽  
Thermostable Direct Hemolysin ◽  
Target Molecules

ABSTRACT Thermostable direct hemolysin (TDH), a major virulence factor of Vibrio parahaemolyticus, induces cytotoxicity in cultured cells. However, the mechanism of TDH's cytotoxic effect including its target molecules on the plasma membrane of eukaryotic cells remains unclear. In this study, we identified the role of lipid rafts, cholesterol- and sphingolipid-enriched microdomains, in TDH cytotoxicity. Treatment of cells with methyl-β-cyclodextrin (MβCD), a raft-disrupting agent, inhibited TDH cytotoxicity. TDH was associated with detergent-resistant membranes (DRMs), and MβCD eliminated this association. In contrast, there was no such association between a nontoxic TDH mutant and DRMs. The disruption of lipid rafts neither affected hemolysis nor inhibited Ca2+ influx into HeLa cells induced by TDH. These findings indicate that the cytotoxicity but not the hemolytic activity of TDH is dependent on lipid rafts. The exogenous and endogenous depletion of cellular sphingomyelin also prevented TDH cytotoxicity, but a direct interaction between TDH and sphingomyelin was not detected with either a lipid overlay assay or a liposome absorption test. Treatment with sphingomyelinase (SMase) at 100 mU/ml disrupted the association of TDH with DRMs but did not affect the localization of lipid raft marker proteins (caveolin-1 and flotillin-1) with DRMs. These results suggest that sphingomyelin is important for the association of TDH with lipid rafts but is not a molecular target of TDH. We hypothesize that TDH may target a certain group of rafts that are sensitive to SMase at a certain concentration, which does not affect other types of rafts.

scholarly journals The role of vitamin D in breast cancer

2011 ◽  
Vol 3 (1) ◽  
pp. 19
Author(s):  
Tu Tu Aung ◽  
Sreenivasa R. Chandana ◽  
Karl J. D’Silva ◽  
Nikolay V. Dimitrov
Keyword(s):  
Breast Cancer ◽  
Vitamin D ◽  
Hormone Receptors ◽  
Therapeutic Agents ◽  
World Population ◽  
Epidemiological Evidence ◽  
Breast Cancer Growth ◽  
Cytochrome P 450 ◽  
Inhibit Cell Proliferation

The biological role of vitamin D outside of calcium homeostasis is still under evaluation. The ability of vitamin D to inhibit cell proliferation and induce differentiation makes it a potential modifier of neoplastic transformation. Vitamin D affects the cell cycle, apoptosis, hormone receptors, angiogenesis, and hypoxia, all of which are related to the breast cancer growth, progression and metastasis. A large percentage of the industrial-world population is deficient in vitamin D. Epidemiological evidence suggests that vitamin D deficiency increases the risk of breast cancer. Vitamin D may have synergistic, additive, or antagonistic effects when combined with other therapeutic agents against breast cancer. Vitamin D appears to depress aromatase inhibitor by acting through cytochrome P 450. This evidence along with pre-clinical and clinical studies, justify the inclusion of vitamin D in future clinical trials related to breast cancer in order to determine its efficacy as a part of the breast cancer therapeutic armament.

scholarly journals The effects of mutational processes and selection on driver mutations across cancer types

2017 ◽  
Author(s):  
Daniel Temko ◽  
Ian PM Tomlinson ◽  
Simone Severini ◽  
Benjamin Schuster-Böckler ◽  
Trevor A Graham
Keyword(s):  
Driver Mutations ◽  
Sequencing Data ◽  
Epidemiological Evidence ◽  
Dna Mismatch ◽  
Cancer Types ◽  
Key Driver ◽  
Independent Effects ◽  
Mutational Processes ◽  
Mutation And Selection

ABSTRACTEpidemiological evidence has long associated environmental mutagens with increased cancer risk. However, links between specific mutation-causing processes and the acquisition of individual driver mutations have remained obscure. Here we have used public cancer sequencing data to infer the independent effects of mutation and selection on driver mutation complement. First, we detect associations between a range of mutational processes, including those linked to smoking, ageing, APOBEC and DNA mismatch repair (MMR) and the presence of key driver mutations across cancer types. Second, we quantify differential selection between well-known alternative driver mutations, including differences in selection between distinct mutant residues in the same gene. These results show that while mutational processes play a large role in determining which driver mutations are present in a cancer, the role of selection frequently dominates.

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