High-resolution spiral real-time cardiac cine imaging with deep learning-based rapid image reconstruction and quantification.

The objective of the current study was to develop and evaluate a DEep learning-based rapid Spiral Image REconstruction (DESIRE) and deep learning (DL)-based segmentation approach to quantify the left ventricular ejection fraction (LVEF) for high-resolution spiral real-time cine imaging, including 2D balanced steady-state free precession imaging at 1.5 T and gradient echo (GRE) imaging at 1.5 and 3 T. A 3D U-Net-based image reconstruction network and 2D U-Net-based image segmentation network were proposed and evaluated. Low-rank plus sparse (L+S) served as the reference for the image reconstruction network and manual contouring of the left ventricle was the reference of the segmentation network. To assess the image reconstruction quality, structural similarity index, peak signal-to-noise ratio, normalized root-mean-square error, and blind grading by two experienced cardiologists (5: excellent; 1: poor) were performed. To assess the segmentation performance, quantification of the LVEF on GRE imaging at 3 T was compared with the quantification from manual contouring. Excellent performance was demonstrated by the proposed technique. In terms of image quality, there was no difference between L+S and the proposed DESIRE technique. For quantification analysis, the proposed DL method was not different to the manual segmentation method (p > 0.05) in terms of quantification of LVEF. The reconstruction time for DESIRE was ~32 s (including nonuniform fast Fourier transform [NUFFT]) per dynamic series (40 frames), while the reconstruction time of L+S with GPU acceleration was approximately 3 min. The DL segmentation takes less than 5 s. In conclusion, the proposed DL-based image reconstruction and quantification techniques enabled 1-min image reconstruction for the whole heart and quantification with automatic reconstruction and quantification of the left ventricle function for high-resolution spiral real-time cine imaging with excellent performance.

Pleiotrophin ameliorates white matter injury of neonatal rats by activating the mTOR/YY1/Id4 signaling pathway.

Brain white matter injury (WMI) is a serious disease of the central nervous system. Pleiotrophin (PTN) promotes the differentiation and myelination of oligodendrocytes (OLs) in vitro. However, the role of PTN in WMI remains unknown. Therefore, this study aimed to investigate the neuroprotective role and potential mechanisms of PTN function in neonatal rats with WMI. The PTN and mammalian target of rapamycin (mTOR) inhibitor everolimus was used to treat a WMI model in postnatal day 3 Sprague-Dawley rats, in which the right common carotid arteries of these rats were isolated, ligated, and exposed to a hypoxic environment (6% O2 + 94% N2 ) for 2 h. OL differentiation and myelination, as well as the spatial learning and memory abilities of the rats were evaluated to examine the effects of PTN. Two proteins of the mTOR signaling pathway, YingYang1 (YY1) and inhibitor of DNA binding 4 (Id4), were detected and were used to explore the potential mechanisms of PTN in rat WMI experiment and oxygen glucose deprivation (OGD) model. We found that the differentiation and myelination of OLs were impaired after WMI. PTN administration rescued this injury by activating mTOR/YY1 and inhibiting Id4. Everolimus administration inhibited mTOR/YY1 and activated Id4, which blocked the neuroprotective role of PTN in WMI. PTN plays a neuroprotective role in neonatal rats with WMI, which could be involved in the mTOR/YY1/Id4 signaling pathway.

Polycyclic pyrroloindoline-containing natural products with a unique 3-heptyl-2a,4a-diazapentaleno[1,6-ab]indene core isolated from Alstonia scholaris.

Alscholarine C (1), featuring an unprecedented pyrroloindoline-containing natural product (PiNP) with a 6/5/5/5 tetracyclic carbon skeleton, and four known PiNPs (2-5), namely demethylalstoscholarinine E (2), Nb-demethylechitamine (3), winphylline A (4), and echitamine (5), were isolated from Alstonia scholaris. Compound 1 was characterized by a hexahydropyrrolo[2,3-b] indole (HPI) core fused to a unique 4-heptylimidazolidine motif, forming an unparalleled 3-heptyl-2a,4a-diazapentaleno[1,6-ab]indene ring system. Their structures were established by spectroscopic analysis, quantum-chemical calculated 13C NMR data with DP4+ probability analyses, and ECD calculations and comparison. A plausible biosynthetic pathway of 1 was proposed. Compound 1 exhibited potential anti-inflammatory activity against LPS-stimulated NO production in RAW264.7 cells.

Construction and evaluation of neonatal respiratory failure risk prediction model for neonatal respiratory distress syndrome.

BACKGROUND: Neonatal respiratory distress syndrome (NRDS) is a common respiratory disease in preterm infants, often accompanied by respiratory failure. The aim of this study was to establish and validate a nomogram model for predicting the probability of respiratory failure in NRDS patients. METHODS: Patients diagnosed with NRDS were extracted from the MIMIC-iv database. The patients were randomly assigned to a training and a validation cohort. Univariate and stepwise Cox regression analyses were used to determine the prognostic factors of NRDS. A nomogram containing these factors was established to predict the incidence of respiratory failure in NRDS patients. The area under the receiver operating characteristic curve (AUC), receiver operating characteristic curve (ROC), calibration curves and decision curve analysis were used to determine the effectiveness of this model. RESULTS: The study included 2,705 patients with NRDS. Univariate and multivariate stepwise Cox regression analysis showed that the independent risk factors for respiratory failure in NRDS patients were gestational age, pH, partial pressure of oxygen (PO2), partial pressure of carbon dioxide (PCO2), hemoglobin, blood culture, infection, neonatal intracranial hemorrhage, Pulmonary surfactant (PS), parenteral nutrition and respiratory support. Then, the nomogram was constructed and verified. CONCLUSIONS: This study identified the independent risk factors of respiratory failure in NRDS patients and used them to construct and evaluate respiratory failure risk prediction model for NRDS. The present findings provide clinicians with the judgment of patients with respiratory failure in NRDS and help clinicians to identify and intervene in the early stage.

Identification of nonfunctional PABPC1L causing oocyte maturation abnormalities and early embryonic arrest in female primary infertility.

Oocyte maturation arrest, fertilization failure, and early embryonic arrest are important causes of female infertility, whereas the genetic events that contribute to these processes are largely unknown. Loss-of-function of PABPC1L in mice has been suggested to cause female infertility involved in the absence of mature oocytes or embryos in vivo or in vitro. However, the role of PABPC1L in human female reproduction remains largely elusive. In this study, we identified a homozygous missense mutation (c.536G>A, p.R179Q) and a compound heterozygous mutation (c.793C>T, p.R265W; c.1201C>T, p.Q401*) in PABPC1L in two unrelated infertile females characterized by recurrent oocyte maturation abnormalities and early embryonic arrest. These variants resulted in nonfunctional PABPC1L protein and were associated with impaired chromatin configuration and transcriptional silencing in GV oocytes. Moreover, the binding capacity of mutant PABPC1L to mRNAs related to oocyte maturation and early embryonic development was decreased significantly. Our findings revealed novel PABPC1L mutations causing oocyte maturation abnormalities and early embryonic arrest, confirming the essential role of PABPC1L in human female fertility.

Atorvastatin inhibits neuronal apoptosis via activating cAMP/PKA/p-CREB/BDNF pathway in hypoxic-ischemic neonatal rats.

Neuronal apoptosis is one of the main pathological processes of hypoxic-ischemic brain damage (HIBD) and is involved in the development of hypoxic-ischemic encephalopathy (HIE) in neonates. Atorvastatin has been found to have neuroprotective effects in some nervous system diseases, but its role in regulating the pathogenesis of neonatal HIBD remains elusive. Thus, this study aimed to explore the effects and related mechanisms of atorvastatin on the regulation of neuronal apoptosis after HIBD in newborn rats. The rat HIBD model and the neuronal oxygen glucose deprivation (OGD) model were established routinely. Atorvastatin, cAMP inhibitor (SQ22536), and BDNF inhibitor (ANA-12) were used to treat HIBD rats and OGD neurons. Cerebral infarction, learning and memory ability, cAMP/PKA/p-CREB/BDNF signaling molecules, and apoptosis-related indicators (TUNEL, cleaved caspase-3, and Bax/Bcl2) were then examined. In vivo, atorvastatin reduced cerebral infarction, improved learning and memory ability, decreased the number of TUNEL-positive neurons, inhibited the expression of cleaved caspase-3 and Bax/Bcl2, and activated the cAMP/PKA/p-CREB/BDNF pathway in the cerebral cortex after HIBD. In vitro, atorvastatin also decreased the apoptosis-related indicators and activated the cAMP/PKA/p-CREB/BDNF pathway in neurons after OGD. Furthermore, inhibition of cAMP or BDNF attenuated the effect of atorvastatin on the reduction of neuronal apoptosis, suggesting that atorvastatin inhibits HIBD-induced neuronal apoptosis and alleviates brain injury in neonatal rats mainly by activating the cAMP/PKA/p-CREB/BDNF pathway. In conclusion, atorvastatin may be developed as a potential drug for the treatment of neonatal HIE.

Alscholarines A and B, two rearranged monoterpene indole alkaloids from Alstonia scholaris.

Alscholarines A and B (1 and 2), two unprecedented rearranged monoterpene indole alkaloids, were isolated from Alstonia scholaris. Alscholarine A (1) features an imidazole ring fused with a rearranged vallesamine-type alkaloid possessing an unparalleled 6/5/6/6 tetracyclic skeleton through an unprecedented C7-C-19 connectivity. Alscholarine B (2), incorporating an unusual 7-oxa-1-azabicyclo[3.2.1]octane moiety, represents a unique rearranged vallesamine-type alkaloid with a 6/5/6/6/5 ring system via an unprecedented C-6-C-20 connectivity. Their structures were established by spectroscopic analysis, X-ray crystallography, and quantum-chemical calculations. Their plausible biosynthetic pathways were proposed. The vasorelaxant and anti-inflammatory activities of them were also evaluated. Compounds 1-3 showed moderate vasorelaxant activities.

Molecular Networking Accelerated Discovery of Biflavonoid Alkaloids from Cephalotaxus sinensis.

Four undescribed biflavonoid alkaloids, sinenbiflavones A-D, were isolated from Cephalotaxus sinensis using a MS/MS-based molecular networking guided strategy. Their structures were elucidated by series of spectroscopic methods (HR-ESI-MS, UV, IR, 1D, and 2D NMR). Sinenbiflavones A-D are the first examples of amentoflavone-type (C-3'-C-8'') biflavonoid alkaloids. Meanwhile, sinenbiflavones B and D are the unique C-6-methylated amentoflavone-type biflavonoid alkaloids. Sinenbiflavone D showed weak SARS-CoV-2 3CLpro inhibitory activity with 43 % inhibition rate at 40 µM.

Free-breathing self-gated continuous-IR spiral T1 mapping: Comparison of dual flip-angle and Bloch-Siegert B1-corrected techniques.

PURPOSE: To develop a B1-corrrected single flip-angle continuous acquisition strategy with free-breathing and cardiac self-gating for spiral T1 mapping, and compare it to a previous dual flip-angle technique. METHODS: Data were continuously acquired using a spiral-out trajectory, rotated by the golden angle in time. During the first 2 s, off-resonance Fermi RF pulses were applied to generate a Bloch-Siegert shift B1 map, and the subsequent data were acquired with an inversion RF pulse applied every 4 s to create a T1* map. The final T1 map was generated from the B1 and the T1* maps by using a look-up table that accounted for slice profile effects, yielding more accurate T1 values. T1 values were compared to those from inversion recovery (IR) spin echo (phantom only), MOLLI, SAturation-recovery single-SHot Acquisition (SASHA), and previously proposed dual flip-angle results. This strategy was evaluated in a phantom and 25 human subjects. RESULTS: The proposed technique showed good agreement with IR spin-echo results in the phantom experiment. For in-vivo studies, the proposed technique and the previously proposed dual flip-angle method were more similar to SASHA results than to MOLLI results. CONCLUSIONS: B1-corrected single flip-angle T1 mapping successfully acquired B1 and T1 maps in a free-breathing, continuous-IR spiral acquisition, providing a method with improved accuracy to measure T1 using a continuous Look-Locker acquisition, as compared to the previously proposed dual excitation flip-angle technique.

Cytotoxic alkaloids from the twigs and leaves of Cephalotaxus sinensis.

Twelve new Cephalotaxus alkaloids (1-12) and nine known analogues (13-21) were isolated and identified from the twigs and leaves of Cephalotaxus sinensis. The structures of the new compounds (1-12) were elucidated by extensive spectroscopic analysis and single-crystal X-ray diffraction analysis. Cephalosine H (8) is the third example of an alkaloid containing the cephalolancine skeleton. Cephalosines J and K (10 and 11) are the rare natural Δ(2)1-alkene-6-hydroxyl homoerythrina-type alkaloids isolated from the Cephalotaxus genus. The racemization of cephalotaxine-type alkaloids is discussed. Alkaloids 6, 7, 11, 16, 18 and 19 exhibited broad and potent cytotoxicities against five human cancer cell lines, with IC50 values ranging from 0.053 to 10.720 µM, highlighting these compounds as promising leads for the development of new antitumor agents.

Metabolites with antioxidant and α-glucosidase inhibitory activities produced by the endophytic fungi Aspergillus niger from Pachysandra terminalis.

One new compound and 13 known compounds were isolated from Aspergillus niger, a plant endophytic fungus of Pachysandra terminalis collected from Qinling Mountains, Xi'an, China. The structure of new compound 1 was classically determined by extensive spectroscopic analysis. Compounds 5, 6, 8, and 14 were first reported from Aspergillus, while compound 2 was isolated from A. niger for the first time. All isolated compounds were further evaluated for their antioxidant and α-glucosidase inhibitory activities. Compounds 2 and 3 exhibited significant antioxidant activities with IC50 values of 31.64 µm and 24.32 µm, respectively, similar to the positive control ascorbic acid. Additionally, compound 1 displayed remarkable inhibitory activity against α-glucosidase with an IC50 value of 96.25 µm, which was 3.4-fold more potent than that of the positive control acarbose. Compound 1 has great potential for development as a new lead compound owing to its simple structure and remarkable biological activity.

Dual-excitation flip-angle simultaneous cine and T1 mapping using spiral acquisition with respiratory and cardiac self-gating.

PURPOSE: To develop a free-breathing cardiac self-gated technique that provides cine images and B1+ slice profile-corrected T1 maps from a single acquisition. METHODS: Without breath-holding or electrocardiogram gating, data were acquired continuously on a 3T scanner using a golden-angle gradient-echo spiral pulse sequence, with an inversion RF pulse applied every 4 seconds. Flip angles of 3° and 15° were used for readouts after the first four and second four inversions. Self-gating cardiac triggers were extracted from heart image navigators, and respiratory motion was corrected by rigid registration on each heartbeat. Cine images were reconstructed from the steady-state portion of 15° readouts using a low-rank plus sparse reconstruction. The T1 maps were fit using a projection onto convex sets approach from images reconstructed using slice profile-corrected dictionary learning. This strategy was evaluated in a phantom and 14 human subjects. RESULTS: The self-gated signal demonstrated close agreement with the acquired electrocardiogram signal. The image quality for the proposed cine images and standard clinical balanced SSFP images were 4.31 (±0.50) and 4.65 (±0.30), respectively. The slice profile-corrected T1 values were similar to those of the inversion-recovery spin-echo technique in phantom, and had a higher global T1 value than that of MOLLI in human subjects. CONCLUSIONS: Cine and T1 mapping using spiral acquisition with respiratory and cardiac self-gating successfully acquired T1 maps and cine images in a single acquisition without the need for electrocardiogram gating or breath-holding. This dual-excitation flip-angle approach provides a novel approach for measuring T1 while accounting for B1+ and slice profile effect on the apparent T1∗ .

High spatial resolution spiral first-pass myocardial perfusion imaging with whole-heart coverage at 3 T.

PURPOSE: To develop and evaluate a high spatial resolution (1.25 × 1.25 mm2 ) spiral first-pass myocardial perfusion imaging technique with whole-heart coverage at 3T, to better assess transmural differences in perfusion between the endocardium and epicardium, to quantify the myocardial ischemic burden, and to improve the detection of obstructive coronary artery disease. METHODS: Whole-heart high-resolution spiral perfusion pulse sequences and corresponding motion-compensated reconstruction techniques for both interleaved single-slice (SS) and simultaneous multi-slice (SMS) acquisition with or without outer-volume suppression (OVS) were developed. The proposed techniques were evaluated in 34 healthy volunteers and 8 patients (55 data sets). SS and SMS images were reconstructed using motion-compensated L1-SPIRiT and SMS-Slice-L1-SPIRiT, respectively. Images were blindly graded by 2 experienced cardiologists on a 5-point scale (5, excellent; 1, poor). RESULTS: High-quality perfusion imaging was achieved for both SS and SMS acquisitions with or without OVS. The SS technique without OVS had the highest scores (4.5 [4, 5]), which were greater than scores for SS with OVS (3.5 [3.25, 3.75], P < .05), MB = 2 without OVS (3.75 [3.25, 4], P < .05), and MB = 2 with OVS (3.75 [2.75, 4], P < .05), but significantly higher than those for MB = 3 without OVS (4 [4, 4], P = .95). SMS image quality was improved using SMS-Slice-L1-SPIRiT as compared to SMS-L1-SPIRiT (P < .05 for both reviewers). CONCLUSION: We demonstrated the successful implementation of whole-heart spiral perfusion imaging with high resolution at 3T. Good image quality was achieved, and the SS without OVS showed the best image quality. Evaluation in patients with expected ischemic heart disease is warranted.

Recombinant CC16 inhibits NLRP3/caspase-1-induced pyroptosis through p38 MAPK and ERK signaling pathways in the brain of a neonatal rat model with sepsis.

BACKGROUND: Sepsis is a critical disease associated with extremely high mortality. Some severe forms of sepsis can induce brain injury, thus causing behavioral and cognitive dysfunction. Pyroptosis is a type of cell death that differs from apoptosis and plays an important role in the occurrence and development of infectious diseases, nervous system-related diseases. A recent study has found that there is pyroptosis in the hippocampus of sepsis-induced brain injury, but its mechanism and treatment scheme have not been evaluated. METHODS: We established immediately a septic rat model by cecal ligation and perforation (CLP) after administration with recombinant club cell protein (rCC16) and/or U46619 in different groups. The clinical performance, survival percentage, vital signs, and neurobehavioral scores were monitored at different time points. Cortical pathological changes were also examined. The expression of cortical nucleotide-binding domain leucine-rich repeat-containing pyrin domain-containing 3 (NLRP3), caspase-1, (p)-p38 mitogen-activated protein kinase (MAPK), and (p)-extracellular signal-related kinase (ERK) was detected by western blotting and immunofluorescence analysis. The levels of interleukin (IL)-1ß, IL-6, and tumor necrosis factor alpha in the cortical supernatant were detected by enzyme-linked immunosorbent assay. RESULTS: Compared with the sham group, the clinical performance, survival percentage, vital signs, and severe cortical pathological changes in the CLP group were worse; NLRP3, caspase-1, and inflammatory factor levels were increased; and phosphorylation of p38 MAPK and ERK was also increased. Meanwhile, multiple indicators were deteriorated further after administration of U46619 in CLP rats. The clinical performance of CLP rats, however, was better after rCC16 administration; cortical pathological changes were attenuated; and NLRP3, caspase-1, and inflammatory factor levels and the phosphorylation of signaling pathway proteins (p38 MAPK and ERK) were reduced. Interestingly, the CLP rats showed the opposite changes in all indicators after administration with both rCC16 and U46619 when compared with those administered rCC16 alone. CONCLUSIONS: In sepsis, rCC16 inhibits cortical pyroptosis through p38 MAPK and ERK signaling pathways. Meanwhile, rCC16 has a protective effect on newborn rats with sepsis, but it is not clear whether its mechanism is directly related to pyroptosis.

Free-breathing cine imaging with motion-corrected reconstruction at 3T using SPiral Acquisition with Respiratory correction and Cardiac Self-gating (SPARCS).

PURPOSE: To develop a continuous-acquisition cardiac self-gated spiral pulse sequence and a respiratory motion-compensated reconstruction strategy for free-breathing cine imaging. METHODS: Cine data were acquired continuously on a 3T scanner for 8 seconds per slice without ECG gating or breath-holding, using a golden-angle gradient echo spiral pulse sequence. Cardiac motion information was extracted by applying principal component analysis on the gridded 8 × 8 k-space center data. Respiratory motion was corrected by rigid registration on each heartbeat. Images were reconstructed using a low-rank and sparse (L+S) technique. This strategy was evaluated in 37 healthy subjects and 8 subjects undergoing clinical cardiac MR studies. Image quality was scored (1-5 scale) in a blinded fashion by 2 experienced cardiologists. In 13 subjects with whole-heart coverage, left ventricular ejection fraction (LVEF) from SPiral Acquisition with Respiratory correction and Cardiac Self-gating (SPARCS) was compared to that from a standard ECG-gated breath-hold balanced steady-state free precession (bSSFP) cine sequence. RESULTS: The self-gated signal was successfully extracted in all cases and demonstrated close agreement with the acquired ECG signal (mean bias, -0.22 ms). The mean image score across all subjects was 4.0 for reconstruction using the L+S model. There was good agreement between the LVEF derived from SPARCS and the gold-standard bSSFP technique. CONCLUSION: SPARCS successfully images cardiac function without the need for ECG gating or breath-holding. With an 8-second data acquisition per slice, whole-heart cine images with clinically acceptable spatial and temporal resolution and image quality can be acquired in <90 seconds of free-breathing acquisition.

[Role of p38 Mitogen-activated Protein Kinase Signaling Pathway in the Hippocampal Neurons Autophagy of Rats with Sepsis].

OBJECTIVE: To investigate the role of p38 mitogen-activated protein kinase (MAPK) signaling pathway in autophagy of neurons in hippocampus of sepsis rats. METHODS: A sepsis model was established by cecal ligation and puncture (CLP). SD rats were randomly divided into sham-operated group (sham group), model group (CLP group), vehicle-treated group (CLP+Veh group) and inhibitor-treated group (CLP+SB203580 group), and each group was divided into 3, 6, 12, 24 and 48 h subgroups. CLP+Veh group and CLP+SB203580 group were injected with 1% DMSO 5 µL and 0.1 mmol/L SB203580 5 µL respectively in the lateral ventricle, and CLP was established 30 min after injection. The sham group only turned over the cecum and closed the abdomen without other treatments. The vital signs of rats were monitored, including mean arterial pressure (MAP) and heart rate (HR). Neurobehavioral score was used to investigate the brain injury in rats. Histopathological changes in hippocampus of rats were observed by HE staining. The process of neuronal autophagy in hippocampal of rats was observed under transmission electron microscope (TEM). Western blot assay was performed to detect the expression of microtubule associated protein 1 light chain 3 (LC3)Ⅱ, LC3Ⅰ, selective autophagy adaptor protein p62/sequestosome-1 (p62/SQSTM1), MAPK-activated protein kinase 2 (MK-2) and phosphorylation MK-2 (p-MK-2) in the hippocampus. The expressions of LC3 and p62/SQSTM1 in hippocampal neurons of rats were observed by immunofluorescence. RESULTS: At different time points, MAP of CLP group was lower than sham group, while HR was higher than sham group, the change was most obvious at 12 h after molding; the neurobehavioral score of CLP group was the lowest; the histopathological changes in the hippocampus were obvious; and many autophagy vacuoles were observed under transmission electron microscope; compared with CLP group, the neurobehavioral score of CLP+SB203580 group increased; the pathological changes in the hippocampus improved; the inclusions in autophagy vacuoles were degraded under transmission electron microscopy; Western blot results showed:compared with sham group, expression of-LC3Ⅱ/LC3Ⅰ, p-MK-2/MK-2 increased, and p62/SQSTM1 decreased in hippocampal tissue of CLP group in rat, the former reaches its peak at 12 h, the latter bottomed out at 12 h. Compared with the other groups, at 12 h of modeling, the expression of LC3Ⅱ/LC3Ⅰ, p-MK-2/MK-2 was further increased, the expression of p62/SQSTM1 decreased further in hippocampal tissue of CLP+SB203580 group in rat (P < 0.05); immunofluorescence observation showed that localization and expression of LC3 and p62/SQSTM1 in NeuN were consistent with Western blot. CONCLUSION: Inhibition of p38 MAPK signaling pathway in sepsis rats can further activate autophagy and protect neurons in the hippocampus.

Simple motion correction strategy reduces respiratory-induced motion artifacts for k-t accelerated and compressed-sensing cardiovascular magnetic resonance perfusion imaging.

BACKGROUND: Cardiovascular magnetic resonance (CMR) stress perfusion imaging provides important diagnostic and prognostic information in coronary artery disease (CAD). Current clinical sequences have limited temporal and/or spatial resolution, and incomplete heart coverage. Techniques such as k-t principal component analysis (PCA) or k-t sparcity and low rank structure (SLR), which rely on the high degree of spatiotemporal correlation in first-pass perfusion data, can significantly accelerate image acquisition mitigating these problems. However, in the presence of respiratory motion, these techniques can suffer from significant degradation of image quality. A number of techniques based on non-rigid registration have been developed. However, to first approximation, breathing motion predominantly results in rigid motion of the heart. To this end, a simple robust motion correction strategy is proposed for k-t accelerated and compressed sensing (CS) perfusion imaging. METHODS: A simple respiratory motion compensation (MC) strategy for k-t accelerated and compressed-sensing CMR perfusion imaging to selectively correct respiratory motion of the heart was implemented based on linear k-space phase shifts derived from rigid motion registration of a region-of-interest (ROI) encompassing the heart. A variable density Poisson disk acquisition strategy was used to minimize coherent aliasing in the presence of respiratory motion, and images were reconstructed using k-t PCA and k-t SLR with or without motion correction. The strategy was evaluated in a CMR-extended cardiac torso digital (XCAT) phantom and in prospectively acquired first-pass perfusion studies in 12 subjects undergoing clinically ordered CMR studies. Phantom studies were assessed using the Structural Similarity Index (SSIM) and Root Mean Square Error (RMSE). In patient studies, image quality was scored in a blinded fashion by two experienced cardiologists. RESULTS: In the phantom experiments, images reconstructed with the MC strategy had higher SSIM (p < 0.01) and lower RMSE (p < 0.01) in the presence of respiratory motion. For patient studies, the MC strategy improved k-t PCA and k-t SLR reconstruction image quality (p < 0.01). The performance of k-t SLR without motion correction demonstrated improved image quality as compared to k-t PCA in the setting of respiratory motion (p < 0.01), while with motion correction there is a trend of better performance in k-t SLR as compared with motion corrected k-t PCA. CONCLUSIONS: Our simple and robust rigid motion compensation strategy greatly reduces motion artifacts and improves image quality for standard k-t PCA and k-t SLR techniques in setting of respiratory motion due to imperfect breath-holding.

Correction to: Simple motion correction strategy reduces respiratory-induced motion artifacts for k-t accelerated and compressed-sensing cardiovascular magnetic resonance perfusion imaging.

Figure 1 of this original publication contained a minor error as one of the lines in the "Reconstruction pipline" was not visible. The updated Fig. 1 is published in this correction article.

G-CSF + plerixafor versus G-CSF alone mobilized hematopoietic stem cells in patients with multiple myeloma and lymphoma: a systematic review and meta-analysis.

AIM: The combination of granulocyte-colony stimulating factor (G-CSF) and plerixafor is one of the approaches for hematopoietic stem cell mobilization in patients with multiple myeloma (MM), non-Hodgkin's lymphoma (NHL), and Hodgkin's lymphoma (HL). This systematic review and meta-analysis aimed to determine the ability of G-CSF + plerixafor to mobilize peripheral blood (PB) CD34+ cells and examine its safety profile. METHODS: We performed a database search using the terms 'granulocyte colony stimulating factor', 'G-CSF', 'AMD3100', and 'plerixafor', published up to May 1, 2023. The methodology is described in further detail in the PROSPERO database (CRD42023425760). RESULTS: Twenty-three studies were included in this systematic review and meta-analysis. G-CSF + plerixafor resulted in more patients achieving the predetermined apheresis yield of CD34+ cells than G-CSF alone (OR, 5.33; 95%, 4.34-6.55). It was further discovered that G-CSF + plerixafor could mobilize more CD34+ cells into PB, which was beneficial for the next transplantation in both randomized controlled (MD, 18.30; 95%, 8.74-27.85) and single-arm (MD, 20.67; 95%, 14.34-27.00) trials. Furthermore, G-CSF + plerixafor did not cause more treatment emergent adverse events than G-CSF alone (OR, 1.25; 95%, 0.87-1.80). CONCLUSIONS: This study suggests that the combination of G-CSF and plerixafor, resulted in more patients with MM, NHL, and HL, achieving the predetermined apheresis yield of CD34+ cells, which is related to the more effective mobilization of CD34+ cells into PB.