Essentially all plant species exhibit heritable genetic variation for resistance to a variety of plant diseases caused by fungi, bacteria, oomycetes or viruses. Disease losses in crop monocultures are already significant, and would be greater but for applications of disease-controlling agrichemicals. For sustainable intensification of crop production, we argue that disease control should as far as possible be achieved using genetics rather than using costly recurrent chemical sprays. The latter imply CO₂ emissions from diesel fuel and potential soil compaction from tractor journeys. Great progress has been made in the past 25 years in our understanding of the molecular basis of plant disease resistance mechanisms, and of how pathogens circumvent them. These insights can inform more sophisticated approaches to elevating disease resistance in crops that help us tip the evolutionary balance in favour of the crop and away from the pathogen. We illustrate this theme with an account of a genetically modified (GM) blight-resistant potato trial in Norwich, using the Rpi-vnt1.1 gene isolated from a wild relative of potato, Solanum venturii, and introduced by GM methods into the potato variety Desiree.
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http://dx.doi.org/10.1098/rstb.2013.0087 | DOI Listing |
Sci Rep
January 2025
Center of Excellence for Antimicrobial Resistance and Stewardship, Department of Microbiology, Faculty of Medicine, Chulalongkorn University, Bangkok, 10330, Thailand.
The pathogenic oomycete Pythium insidiosum causes a fatal infectious illness known as pythiosis, impacting humans and certain animals in numerous countries in the tropics and subtropics. Delayed diagnosis is a primary factor contributing to the heightened morbidity and mortality associated with the disease. Several new serodiagnostic methods have been developed to improve the identification of pythiosis.
View Article and Find Full Text PDFBackground: The association between serum uric acid (SUA) and dyslipidaemia is still unclear in patients with type 2 diabetes mellitus (T2DM). This study aimed to examine the association between SUA and dyslipidaemia and to explore whether there is an optimal SUA level corresponding to the lower risk of suffering from dyslipidaemia.
Research Design And Methods: This cross-sectional study included 1036 inpatients with T2DM and the clinical data were extracted from the hospital medical records.
Trends Endocrinol Metab
January 2025
School of Public Health and Preventive Medicine, Monash University, Melbourne, VIC, Australia.
With the rising prevalence of type 2 diabetes mellitus (T2DM) and obesity, several previously under-recognised complications associated with T2DM are becoming more evident. The most common of these emerging complications are metabolic dysfunction-associated steatotic liver disease (MASLD), cancer, dementia, sarcopenia, and frailty, as well as other conditions involving the lung, heart, and intestinal tract. Likely causative factors are chronic inflammation and insulin resistance, whereas blood glucose levels appear to play a lesser role.
View Article and Find Full Text PDFEnviron Pollut
January 2025
School of Medicine, Taizhou University, Taizhou 318000, China.
Allergic asthma is a significant international concern in respiratory health, which can be exacerbated by the increasing levels of non-allergenic pollutants. This rise in airborne pollutants is a primary driver behind the growing prevalence of asthma, posing a health emergency. Additionally, climatic risk factors can contribute to the onset and progression of asthma.
View Article and Find Full Text PDFEnviron Pollut
January 2025
Department of Toxicology, School of Public Health, Hebei Medical University, Shijiazhuang, 050017, PR China; Hebei Key Laboratory of Environment and Human Health, Hebei Province, Shijiazhuang, 050017, PR China. Electronic address:
Perfluorooctane sulfonate (PFOS), a prevalent perfluoroalkyl substance (PFAS), is widely present in various environmental media, animals, and even human bodies. It primarily accumulates in the liver, contributing to the disruption of hepatic metabolic homeostasis. However, the precise mechanism underlying PFOS-induced hepatic glucolipid metabolic disorders remains elusive.
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