No abstract

Legumes have adaptive mechanisms that regulate nodulation in response to the amount of nitrogen in the soil. In Lotus japonicus, two NODULE INCEPTION (NIN)-LIKE PROTEIN (NLP) transcription factors, LjNLP4 and LjNLP1, play pivotal roles in the negative regulation of nodulation by controlling the expression of symbiotic genes in high nitrate conditions. Despite an improved understanding of the molecular basis for regulating nodulation, how nitrate plays a role in the signaling pathway to negatively regulate this process is largely unknown. Here, we show that nitrate transport via NITRATE TRANSPORTER 2.1 (LjNRT2.1) is a key step in the NLP signaling pathway to control nodulation. A mutation in the LjNRT2.1 gene attenuates the nitrate-induced control of nodulation. LjNLP1 is necessary and sufficient to induce LjNRT2.1 expression, thereby regulating nitrate uptake/transport. Our data suggest that LjNRT2.1-mediated nitrate uptake/transport is required for LjNLP4 nuclear localization and induction/repression of symbiotic genes. We further show that LjNIN, a positive regulator of nodulation, counteracts the LjNLP1-dependent induction of LjNRT2.1 expression, which is linked to a reduction in nitrate uptake. These findings suggest a plant strategy in which nitrogen acquisition switches from obtaining nitrogen from the soil to symbiotic nitrogen fixation.

Most children with grade 2 or 3 PVL had severe neurodevelopmental delays, but attention should also be paid to the 56% of children with grade 1 PVL who presented with normal psychomotor development. Further studies of larger populations, including long-term follow-up, are necessary to evaluate the outcomes of children with PVL.

The present study investigated the physiologic and sedative effects between two different continuous infusion doses of dexmedetomidine (DEX). Thirteen subjects were separately sedated with DEX at a continuous infusion dose of 0.2 µg/kg/hr for 25 minutes after a loading dose of 6 µg/kg/hr for 5 minutes (0.2 group) and a continuous infusion dose of 0.4 µg/kg/hr for 25 minutes after a loading dose of 6 µg/kg/hr for 5 minutes (0.4 group). The recovery process was then observed for 60 minutes post infusion. The tidal volume, mean arterial pressure, and heart rate in both groups decreased significantly during infusion, but they were within a clinically acceptable level. A Trieger dot test plot error ratio in the 0.4 group was significantly higher than that in the 0.2 group until 15 minutes post infusion. Sedation appears to be safe at the infusion doses of DEX studied. However, increasing maintenance infusion doses of DEX from 0.2 µg/kg/hr to 0.4 µg/kg/hr delays some recovery parameters.

Trunk muscles may not be able to function appropriately when individuals lift an object that is much heavier than expected.