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Impaired proinflammatory cytokine production without any reduction in cytokine mRNA levels in tnc− / − cells led us to investigate whether tnc− / − BMDMs exhibit abnormal intracellular cytokine levels as a consequence of deficient secretion.
As a consequence of deficient financing, physicians face limitations in decision-making and fibrinolysis in ACS with persistent ST-elevation is applied relatively rarely and depends more on the hospital's actual budget situation than on patients' medical needs.
In fact, patients suffering from the X-linked hyperimmunoglobulin-M syndrome, which results from a genetic mutation in the CD154 gene, fail to produce the immunoglobulins IgG, IgA and IgE as a consequence of deficient CD40 signaling in B cells [ 9].
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However, it is unlikely that the phenotype we observe in the absence of Shh signaling is a consequence of deficient Slit expression, as, in fact, mice deficient in Slit1 and Slit2 display the opposite phenotype: ventrally displaced ascending dopaminergic fibers, with a relative expansion of the medial fibers that course ventrally [3].
Thus, deficient object categorization might be a consequence of deficient association formation in schizophrenia.
The somatic mutations that affected the GCG repeat in this study are a consequence of deficient MMR function.
This result hints that reoxygenation did not occur as a consequence of the deficient vasculature of tumours [ 49].
From this perspective, men's propensity to die at a younger age than women is commonly explained as a consequence of their deficient behaviour and lifestyle [ 7].
Thus, observing no overt spontaneous phenotypes as a consequence of combined deficiency of Mmp13 and Plau, we next initiated a wound healing study in which we inflicted standardized 20 mm-long full-thickness incisional skin wounds on wild-type (n = 15), Mmp13-deficient (n = 19), Plau-deficient (n = 16) and Mmp13 Plau double-deficient (n = 15) mice.
It has been demonstrated that, when BER is inactivated (e.g. as a consequence of PARP1 inhibition), BRCA-deficient cells are unable to repair the DSBs that evolve from SSBs, and this leads to deadly defects in the genome (Bryant et al, 2005; Farmer et al, 2005).
As a consequence of these medullary lesions, Ar-deficient mice develop a phenotype resembling that of nephrogenic diabetes insipidus in human [ 34, 35].
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