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Total oxysterols significantly decreased as HO-1 expression increased in GFAP.HMOX1 mice expressing high levels of HO-1, whereas total oxysterols increased as HO-1 expression increased in aged 3xTg-AD mice.
A complementary DNA encoding the human low density lipoprotein (LDL) receptor under control of the mouse metallothionein-I promoter was injected into fertilized mouse eggs, and a strain of mice expressing high levels of LDL receptors was established.
Primary myocytes isolated from transgenic mice expressing high levels of α-syntrophin (on the α-syntrophin null background) show a high level of myogenin expression during differentiation.
Indeed, transgenic mice expressing high levels of WSX1 in MLR/lpr background rendered the autoimmune-prone mice protected from the development of autoimmune disease [32].
As shown in Figure 6C, significant higher percentage of BMDCs derived from Stat5-Tg mice expressing high levels of MHC-II and costimulatory molecules such as CD80, CD86 and CD54 before and after LPS stimulation, as compared with their control littermates.
By contrast, mice expressing high levels of DDIT3, which lacks the FUS domain, were not able to develop any tumor despite its tumorigenicity in vitro [19] although the co-expression of the FUS domain was able to restore liposarcoma development suggesting that it plays a critical role in the pathogenesis of liposarcoma [22].
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The disparate ethanol drinking behaviors of B6 mice expressing high-drinking/preference and D2 mice expressing low-drinking/preference have yielded considerable insight into the heritable control of alcohol drinking.
Transgenic mice expressing higher levels of miR-499 (line #9 or TG-9) developed enlarged hearts (n = 16) as demonstrated by gross pathology at 5 weeks of life (Fig. 2B).
In contrast, when a similar analysis was performed in dtg mice expressing higher frequency of Tregs, we found that the induction of both CCL2 and CCL3 after immunization was significantly suppressed, and this was not the case for CCL5 (Fig. 3B).
Therefore, the development of mice expressing higher levels of mutated trypsinogen may offer the opportunity to replicate the human disease.
However, a recent report describes degeneration of a subset of motor neurons in mice expressing higher levels of the VAPB-P56S transgene (Aliaga et al., 2013).
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