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Emerging details of disease pathogenesis support the current concept that ongoing immune activation in IBD is driven by bacterial microbiota, possibly as a result to an attenuated antimicrobial barrier in genetically predisposed individuals [1] [3].
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The discovery of the link between amyloid formation and prostate pathogenesis supports the paradigm that the generic ability of polypeptides to assembly into this stable form as an alternative to the native state [70], [71] is likely to result in its involvement in an increasing number of age-related diseases.
As in the prior study 17, the TERT rs2736100_C association was present in PV, ET, and PMF, implying a general role in MPN pathogenesis (Supporting Information Table 1).
Overall, this study suggests that cigarette smoke may promote C. albicans pathogenesis, supporting both the increased persistence of this pathogen in smokers and the severity of candidiasis.
Thus, our findings highlight the potential role played by damaged mitochondria accumulation in HD pathogenesis, and support the PINK1/Parkin pathway as a valuable therapeutic target.
Recent research has thus focused on investigating the molecular and cellular pathways and processes involved in AD pathogenesis to support the development of effective disease-modifying agents.
Further studies using this model are likely to provide insights into disease pathogenesis and support the development of more targeted treatments for inflammatory disorders.
Molecular genetic studies in familial forms of the disease identified key proteins involved in PD pathogenesis, and support a major role for mitochondrial dysfunction, which is also of significant importance to the common sporadic forms of PD.
The inclusion of temporal and spatial parameters enables mathematical modelling (often referred to as "systems biology"), which may produce new insights into the mechanisms of pathogenesis and support the development of novel therapies [ 1].
The etiology of Takayasu arteritis remains poorly understood, but genetic contribution to the disease pathogenesis is supported by the genetic association with HLA-B∗52.
Although these cells may help in the containment of the bacilli during the initial phase of infection, their involvement in TB pathogenesis is supported by a number of studies.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com