Group A1 heat shock transcription factors (HsfA1s) are the master regulators of the heat stress response (HSR) in plants. Upon heat shock, HsfA1s trigger a transcriptional cascade that is composed of many transcription factors. Despite the importance of HsfA1s and their downstream transcriptional cascade in the acquisition of thermotolerance in plants, the molecular basis of their activation remains poorly understood. Here, domain analysis of HsfA1d, one of several HsfA1s in Arabidopsis thaliana, demonstrated that the central region of HsfA1d is a key regulatory domain that represses HsfA1d transactivation activity through interaction with HEAT SHOCK PROTEIN70 (HSP70) and HSP90. We designated this region as the temperature-dependent repression (TDR) domain. We found that HSP70 dissociates from HsfA1d in response to heat shock and that the dissociation is likely regulated by an as yet unknown activation mechanism, such as HsfA1d phosphorylation. Overexpression of constitutively active HsfA1d that lacked the TDR domain induced expression of heat shock proteins in the absence of heat stress, thereby conferring potent thermotolerance on the overexpressors. However, transcriptome analysis of the overexpressors demonstrated that the constitutively active HsfA1d could not trigger the complete transcriptional cascade under normal conditions, thereby indicating that other factors are necessary to fully induce the HSR. These complex regulatory mechanisms related to the transcriptional cascade may enable plants to respond resiliently to various heat stress conditions.
Wide variability exists in the prediction of intracranial aneurysm WSS. While segmentation and CFD solver techniques may be difficult to standardize across groups, our findings suggest that some of the variability in image-based CFD could be reduced by establishing guidelines for model extents, inflow rates, and blood properties, and by encouraging the reporting of normalized hemodynamic parameters.
In our experience, the clinical features of SCAD appear to be similar to those reported previously. SCAD appears to be rare, but it should be considered in ACS patients, especially in younger females.
Background
Although perfusion imaging plays a key role in the management of steno‐occlusive diseases, the clinical usefulness of arterial spin labeling (ASL) is limited by technical issues.
Purpose
To examine the effect of arterial transit time (ATT) prolongation on cerebral blood flow (CBF) measurement accuracy and identify the best CBF measurement protocol for steno‐occlusive diseases.
Study Type
Prospective.
Population
Moyamoya (n = 10) and atherosclerotic diseases (n = 8).
Field Strength/Sequence
A 3.0T/3DT1‐weighted and ASL.
Assessment
Hadamard‐encoded multidelay ASL scans with/without vessel suppression (VS) and single‐delay ASL scans with long‐label duration (LD) and long postlabeling delay (PLD), referred to as long‐label long‐delay (LLLD), were acquired. CBF measurement accuracy and its ATT dependency, measured as the correlation between the relative CBF measurement difference (ASL—single‐photon emission computed tomography [SPECT]) and ATT, were compared among 1) Combo (incorporating multidelay and LLLD data based on ATT), 2) standard (LD/PLD = 1333/2333 msec), and 3) LLLD (LD/PLD = 4000/4000 msec) protocols, using whole‐brain voxel‐wise correlation with reference standard SPECT CBF. The effect of VS on CBF measurement accuracy was also assessed.
Statistical Tests
Pearson's correlation coefficient, repeated‐measures analysis of variance, t‐test. P< 0.05 was considered significant.
Results
Pearson's correlation coefficients between ASL and SPECT CBF measurements were as follows: Combo = 0.55 ± 0.09; standard = 0.52 ± 0.12; LLLD = 0.41 ± 0.10. CBF measurement was least accurate in LLLD and most accurate in Combo. VS significantly improved overall CBF measurement accuracy in the standard protocol and in moyamoya patients for the Combo. ATT dependency analysis revealed that, compared with Combo, the standard and LLLD protocols showed significantly lower and negative and significantly higher and positive correlations, respectively (standard = −0.12 ± 0.04, Combo = −0.04 ± 0.03, LLLD = 0.17 ± 0.03).
Data Conclusion
By using ATT‐corrected CBF derived from LD/PLD = 1333/2333 msec as a base and by compensating underestimation in delayed regions using multidelay scans, the ATT‐based Combo strategy improves CBF measurement accuracy compared with single‐delay protocols in severe steno‐occlusive diseases.
Evidence Level
1
Technical Efficacy
Stage 2
We identify possible differences in the cytokine/chemokine profiles in cerebrospinal fluid (CSF) from children with encephalopathy and febrile seizure. Interleukin (IL)‐1β, 2, 4, 5, 6, 7, 8, 10, 12, 13, 17, interferon‐γ, tumour necrosis factor‐α, granulocyte colony‐stimulating factor, granulocyte monocyte colony‐stimulating factor, monocyte chemoattractant protein‐1 and macrophage inflammatory protein‐1β were measured simultaneously in CSF supernatants from children with encephalopathy (n = 8), febrile seizure (n = 16) and fever without neurological complications (n = 8). IL‐8 in CSF from children with encephalopathy was significantly elevated compared to that in CSF from children with febrile seizure and fever without neurological complications. IL‐8 in CSF was also higher than serum IL‐8, suggesting that increased IL‐8 was generated from glia cells or astrocytes, not by leakage from serum. Increased IL‐8 in CSF in encephalopathy may protect against severe brain damage.
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