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It has been speculated that alterations in the synthesis or degradation of membrane components might contribute to such changes, and thereby to initiation and progression of nephritis through facilitation of immune complex deposition.
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It has been speculated that this aspect may be secondary to menopause-induced alterations in hormonal balance, in particular the reduction of estrogen levels and the decrease of estradiol/testosterone ratio.
It has been speculated that mutations in TRPC6 may result in apoptosis, podocyte detachment or an alteration in the ultrafiltration coefficient [ 12, 13].
It could be speculated that the alterations in arginine and citrulline levels related to genetic variations in CPS1 function may be only present later in life, under the NEC stress conditions, when the demand for NO might suddenly increase.
It may be speculated that these alterations contributed to the maldigestion and malnutrition and also the decreased feed intake and loss of body weight in the goats [ 18]. [ 16] reported that plasma insulin levels were increased in rats with Cu deficiency, more in female than in male animals.
It is speculated that additional genomic alteration(s) are required for the pathophysiology of PTCL having STX11 alteration.
Therefore, it could be speculated that an early alteration of insulin secretion may represent the stronger predictive factor for the development of diabetes in PCOS patients as pregnancy proceeds.
It has been recognized that the interaction between tumors cells and the stromal compartment may play a significant role in cancer progression/proliferation. It is speculated that tumor development is caused by genetic alterations, in part, and tumor progression results from communication between neoplastic cells and their microenvironment [ 9].
It is speculated that this is a contributing mechanism for the programmed alterations in offspring metabolism associated with increased adiposity and insulin resistance.
Nevertheless, since alterations in adult neurogenesis have been repeatedly shown in various animal models of these disorders [ 70] (Table 1), it is speculated that cognitive decline in neurodegenerative diseases could be partly due to alterations in the neurogenic process.
Based on these findings, it can be speculated that such an interplay could be at the basis of mesenchymal alterations giving rise to skeletal, cardiac, and hemopoietic abnormalities observed in NS and other RASopathies.
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