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We hypothesize that tumor-derived TGF-β (td-TGF-β) plays an important role in maintaining tumor remission by controlling tumor proliferation in vivo, and that decreasing td-TGF-β in the tumor microenvironment will result in tumor progression.

Based on the model of climate controlling fluvial cycles in the Beijing Plain, we suggest that the higher inputs of magnetic minerals, as a result of increasing precipitation, resulted in higher values of k and SIRM in the interglacial periods and that decreasing precipitation in the glacial periods reduced the inputs of magnetic minerals, resulting in lower values of k and SIRM.

We found that the expression of Kir7.1 was regulated in pregnancy and that decreasing Kir7.1 activity in vitro and in vivo greatly increased uterine activity.

The idea that oxidative stress is pathological in the context of these diseases, and that decreasing oxidative stress is therefore a likely therapeutic strategy, has become a paradigm in the field.

Subsequent prospective studies showed that at diagnosis of haemorrhage, platelet counts in PPH patients were significantly lower than those in healthy parturients, and that decreasing platelet count during obstetric bleeding may be associated with progression to severe PPH.

Nevertheless our data demonstrates that S1P production controlled by SPHK1 and SGPL1 are key determinants of cytotoxic drug resistance and that decreasing S1P production in cancer cells could lead to increased cytotoxic sensitivity.

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We hypothesized that VDAC isoforms modulate eNOS activity in the pulmonary circulation, and that decreased VDAC expression contributes to PPHN.

Our finding that Nampt+/− mice were protected against bone erosion in CIA led us to hypothesize that Nampt plays a critical role in osteoclast differentiation and that decreased Nampt expression attenuates osteoclast formation.

Numerical, the condition (45) clears in Fig. 4, where the counterpart values of Fig. 3 are greater than zero and that decreases as k decreases.

Specifically we have demonstrated that regulating type III TGF-ß receptor expression levels is sufficient to regulate TGF-ß signaling, and that decreased type III receptor expression is a common phenomenon in human cancers, resulting in cancer progression.

Based on these observations we hypothesized that SAE is decreased in SLE patients and that decreased SAE is related to non-traditional risk factors, including AGEs.

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