Myocardial Injury in Peritoneal Dialysis Patients Assessed by Multiparametric MRI: Relationship With Left Ventricular Phenotypes.

BACKGROUND: Myocardial injury is common in end-stage renal disease (ESRD) patients, but the presence and severity of myocardial injury in different left ventricular (LV) phenotypes were still not fully explored. PURPOSE: To evaluate myocardial tissue characteristics and deformation in ESRD patients on peritoneal dialysis separated into normal geometry, concentric remodeling, concentric left ventricular hypertrophy (LVH) and eccentric LVH patterns by multiparametric cardiac MRI. STUDY TYPE: Prospective. POPULATION: A total of 142 subjects, including 102 on peritoneal dialysis (69 males) and 40 healthy controls (27 males). FIELD STRENGTH/SEQUENCE: At 3.0 T, cine sequence, T1 mapping and T2 mapping. ASSESSMENT: LV mass index and LV remodeling index were used to create four subgroups with normal geometry, concentric remodeling, concentric LVH, and eccentric LVH. LV function, strain and strain rate, myocardial native T1 and T2 were measured. STATISTICAL TESTS: Descriptive statistics, analysis of variance and analysis of covariance, Pearson/Spearman correlation, stepwise regression, and intraclass correlation coefficient. P-value <0.05 was considered statistically significant. RESULTS: Even in normal geometry, LV strain parameters still diminished compared with the controls (global radial strain: 30.5 ± 7.7% vs. 37.1 ± 7.9%; global circumferential strain: -18.2 ± 2.6% vs. -20.6 ± 2.2%; global longitudinal strain: -13.3 ± 2.5% vs. -16.0 ± 2.8%). Eccentric LVH had significantly lower global circumferential systolic strain rate than concentric LVH (-0.82 ± 0.21%/- second vs. -0.96 ± 0.20%/- second). Compared with the controls, the four subgroups all revealed elevated native T1 and T2, especially in eccentric LVH, while concentric remodeling had the least changes including native T1, T2, and LV ejection fraction. After adjusting for covariates, there was no statistically significant difference in T2 between the four subgroups (P = 0.359). DATA CONCLUSIONS: Eccentric LVH is associated with the most pronounced evidence of myocardial tissue characteristics and function impairment, while as a benign remodeling, the concentric remodeling subgroup had the least increase in native T1. This study further confirms that native T1 and strain indicators can reflect the severity of myocardial injury in ESRD, providing better histological and functional basis for future grouping treatments. LEVEL OF EVIDENCE: 1 TECHNICAL EFFICACY: Stage 3.

Serial Cardiac MRI for Quantification of the Dynamics of Anthracycline-Induced Subclinical Myocardial Injury.

BACKGROUND: Anthracyclines are known to be associated with chemotherapy-induced cardiotoxicity. Limited data focus on dynamic myocardial injury during the course of chemotherapy in patients with breast cancer. PURPOSE: To investigate the variation of tissue characterization and myocardial deformation derived by cardiac MRI during anthracycline chemotherapy. STUDY TYPE: Prospective. POPULATION: Fifty-eight female breast cancer patients (mean age: 52.82 ± 2.61 years) were enrolled. FIELD STRENGTH/SEQUENCE: A 3.0-T, cardiac MRI including cine balanced steady-state free precession, a modified Looker-Locker inversion recovery (MOLLI), and a fast spin echo (FSE) T2-weighted sequences were performed. ASSESSMENT: Cardiac MRI was performed baseline and after two, four, and six cycles of chemotherapy. Assessment of global longitudinal strain (GLS), global circumstance strain (GCS), global radial strain (GRS), and strain rate (GLS-s, GCS-s, GRS-s) and T1, T2 and T2* were accomplished by CVI42. The anthracycline dose and risk factors were also collected before each cardiac MRI. STATISTICAL TESTS: Analysis of variance (ANOVA) for repeated measures was used to compare the changes in LVEF cardiac function, strain and T1/T2/T2* parameters over time. Pearson correlation analyses were performed to estimate the potential associations between differences in myocardial characteristics (∆) and the chemotherapy cycle. A P value <0.05 was considered statistically significant. RESULTS: LVEF was not significantly different from pretreatment MRI regarding each cycle of chemotherapy (P = 0.54). Compared with baseline, patients had significantly lower GLS (-15.85% ± 0.83%, -14.50% ± 0.88%, -12.34% ± 1.01% vs. -18.82% ± 0.92%) and GLS-s (-0.71% ± 0.07%, -0.65% ± 0.05%, -0.64% ± 0.04% vs. -0.95 ± 0.06%) and increased T2 values (57.21 ± 4.27 msec, 58.60 ± 3.93 msec, 58.10 ± 3.17 msec vs. 43.88 ± 3.28 msec) at two, four and six cycles of chemotherapy treatment. ∆GLS and ∆GLS-s were significantly associated with the chemotherapy cycle (correlation coefficients for GLS = 0.75, GLS-s = 0.75). DATA CONCLUSION: Cardiac MRI can precisely detect the dynamic changes of anthracycline-induced subclinical myocardial injury that is represented as a gradually decrease in GLS and GLS-s. These parameters may provide new insight for monitoring risk and therapy in patients with breast cancer. EVIDENCE LEVEL: 2. TECHNICAL EFFICACY: Stage 1.

Coronary CTA-based radiomic signature of pericoronary adipose tissue predict rapid plaque progression.

OBJECTIVES: To explore the value of radiomic features derived from pericoronary adipose tissue (PCAT) obtained by coronary computed tomography angiography for prediction of coronary rapid plaque progression (RPP). METHODS: A total of 1233 patients from two centers were included in this multicenter retrospective study. The participants were divided into training, internal validation, and external validation cohorts. Conventional plaque characteristics and radiomic features of PCAT were extracted and analyzed. Random Forest was used to construct five models. Model 1: clinical model. Model 2: plaque characteristics model. Model 3: PCAT radiomics model. Model 4: clinical + radiomics model. Model 5: plaque characteristics + radiomics model. The evaluation of the models encompassed identification accuracy, calibration precision, and clinical applicability. Delong' test was employed to compare the area under the curve (AUC) of different models. RESULTS: Seven radiomic features, including two shape features, three first-order features, and two textural features, were selected to build the PCAT radiomics model. In contrast to the clinical model and plaque characteristics model, the PCAT radiomics model (AUC 0.85 for training, 0.84 for internal validation, and 0.81 for external validation; p < 0.05) achieved significantly higher diagnostic performance in predicting RPP. The separate combination of radiomics with clinical and plaque characteristics model did not further improve diagnostic efficacy statistically (p > 0.05). CONCLUSION: Radiomic feature analysis derived from PCAT significantly improves the prediction of RPP as compared to clinical and plaque characteristics. Radiomic analysis of PCAT may improve monitoring RPP over time. CRITICAL RELEVANCE STATEMENT: Our findings demonstrate PCAT radiomics model exhibited good performance in the prediction of RPP, with potential clinical value. KEY POINTS: Rapid plaque progression may be predictable with radiomics from pericoronary adipose tissue. Fibrous plaque volume, diameter stenosis, and fat attenuation index were identified as risk factors for predicting rapid plaque progression. Radiomics features of pericoronary adipose tissue can improve the predictive ability of rapid plaque progression.

Polybrominated diphenyl ethers in human hair from the college environment: comparison with indoor dust.

Eight Polybrominated diphenyl ether (PBDE) congeners (BDE 28, 47, 99, 100, 153, 154, 183 and 209) were determined to examine the hair burden at low concentrations, and the relationship between PBDE concentrations in human hair and indoor dust from a college environment (Shanghai University campus). Chemical analyses showed that the total concentrations of PBDEs in hair ranged from 4.04 to 99 ng/g dw, and were found to be fourfold higher in females than in males (p < 0.05). The total PBDEs concentrations in indoor dust samples ranged from 170 to 1,360 ng/g dw. Significantly positive correlations were observed between human hair and indoor dust for BDE 47 (r = 0.44, p = 0.048) and BDE 99 (r = 0.68, p = 0.025). However, no significant association was noted between other PBDE congeners in human hair and indoor dust in the present study.

Heart failure with preserved ejection fraction in post myocardial infarction patients: a myocardial magnetic resonance (MR) tissue tracking study.

Background: This study aimed to explore the value of cardiac magnetic resonance tissue tracking (CMR-TT) technology in evaluating heart failure with preserved ejection fraction (HFpEF) in patients with chronic myocardial infarction (CMI). Methods: Between June 2016 and March 2022, we included a consecutive series of 92 patients with CMI and 40 healthy controls in this retrospective study. The CMI patients enrolled were divided into different subgroups [HFpEF-CMI group (n=54) and non- heart failure (HF)-CMI group (n=38)] according to the Heart Failure Association (HFA)-PEFF (step 1: P, pre-test assessment; step 2: E, echocardiography and natriuretic peptide score; step 3: F1, functional testing; step 4: F2, final aetiology) diagnostic algorithm. CMR scan was performed at the First Hospital of China Medical University. Quantitative measurements of myocardial damage, such as myocardial strain parameters of both ventricles derived by CMR-TT and infarct size and transmurality by late gadolinium enhancement (LGE), were assessed. One-way analysis of variance, independent samples t-test, and rank sum test were used to compare myocardial impairment among groups. Pearson or Spearman correlation coefficient was used to measure correlations between left ventricular (LV) strains and clinical and functional parameters. Logistic regression analysis and receiver operating characteristic (ROC) curve were performed to identify the best parameter for diagnosing HFpEF-CMI. Results: HFpEF-CMI patients demonstrated significantly impaired LV strains and strain rates in all of the three directions (radial, circumferential and longitudinal) compared to non-HF-CMI patients and healthy controls (P<0.001 for all), whereas only global longitudinal strain (GLS) was significantly impaired in HFpEF-CMI patients vs. controls for right ventricular strain parameters (P<0.001). LV strains showed moderate correlation with N-terminal pro-brain natriuretic peptide (radial, circumferential and longitudinal strain, R=-0.401, R=0.408, R=0.407, respectively, P<0.001 for all). LV strains in the three directions (radial, circumferential and longitudinal) [area under ROC curve (AUC) =0.707, 95% confidence interval (CI): 0.603-0.797; AUC =0.708, 95% CI: 0.604-0.798; AUC =0.731, 95% CI: 0.628-0.818; respectively, P<0.01 for all] were discriminators for HFpEF-CMI and non-HF-CMI. LV strains and myocardial infarction volume were independent factors in multi-logistic regression analysis after adjusting for body mass index, age, and sex (P<0.05 for all). Conclusions: CMR-TT provides clinicians with useful additional imaging parameters to facilitate the assessment of CMI patients with HFpEF. LV strain parameters can detect early cardiac insufficiency in patients with HFpEF-CMI and have potential value for discriminating between HFpEF and non-HF patients post-CMI.

CUL4B orchestrates mesenchymal stem cell commitment by epigenetically repressing KLF4 and C/EBPδ.

Dysregulated lineage commitment of mesenchymal stem cells (MSCs) contributes to impaired bone formation and an imbalance between adipogenesis and osteogenesis during skeletal aging and osteoporosis. The intrinsic cellular mechanism that regulates MSC commitment remains unclear. Here, we identified Cullin 4B (CUL4B) as a critical regulator of MSC commitment. CUL4B is expressed in bone marrow MSCs (BMSCs) and downregulated with aging in mice and humans. Conditional knockout of Cul4b in MSCs resulted in impaired postnatal skeletal development with low bone mass and reduced bone formation. Moreover, depletion of CUL4B in MSCs aggravated bone loss and marrow adipose accumulation during natural aging or after ovariectomy. In addition, CUL4B deficiency in MSCs reduced bone strength. Mechanistically, CUL4B promoted osteogenesis and inhibited adipogenesis of MSCs by repressing KLF4 and C/EBPδ expression, respectively. The CUL4B complex directly bound to Klf4 and Cebpd and epigenetically repressed their transcription. Collectively, this study reveals CUL4B-mediated epigenetic regulation of the osteogenic or adipogenic commitment of MSCs, which has therapeutic implications in osteoporosis.

CRL4B complex-mediated H2AK119 monoubiquitination restrains Th1 and Th2 cell differentiation.

CD4+ T helper (Th) cell differentiation is regulated by lineage-specific expression of transcription factors, which is tightly associated with epigenetic modifications, including histone acetylation and methylation. However, the factors regulating histone modifications involved in Th cell differentiation remain largely unknown. We herein demonstrated a critical role of Cullin 4B (CUL4B) in restricting Th1 and Th2 cell differentiation. CUL4B, which is assembled into the CUL4B-RING E3 ligase (CRL4B) complex, participates in various physiological and developmental processes through epigenetic repression of transcription. Depletion of Cul4b in CD4+ T cells enhanced Th1 and Th2 cell differentiation. In vivo, an aggravated Th2 response caused by the absence of CUL4B was observed in a murine asthma model. Mechanistically, the CRL4B complex promoted monoubiquitination at H2AK119 (H2AK119ub1) and polycomb repressive complex 2 (PRC2)-mediated trimethylation at H3K27 (H3K27me3) at Tbx21 and Maf and consequently repressed their expression during Th cell differentiation. Our study suggests that CRL4B complex-mediated H2AK119ub1 deposition functions to prevent the aberrant expression of Th1 and Th2 lineage-specific genes.

Depletion of CUL4B in macrophages ameliorates diabetic kidney disease via miR-194-5p/ITGA9 axis.

Diabetic kidney disease (DKD) is the most prevalent chronic kidney disease. Macrophage infiltration in the kidney is critical for the progression of DKD. However, the underlying mechanism is far from clear. Cullin 4B (CUL4B) is the scaffold protein in CUL4B-RING E3 ligase complexes. Previous studies have shown that depletion of CUL4B in macrophages aggravates lipopolysaccharide-induced peritonitis and septic shock. In this study, using two mouse models for DKD, we demonstrate that myeloid deficiency of CUL4B alleviates diabetes-induced renal injury and fibrosis. In vivo and in vitro analyses reveal that loss of CUL4B suppresses migration, adhesion, and renal infiltration of macrophages. Mechanistically, we show that high glucose upregulates CUL4B in macrophages. CUL4B represses expression of miR-194-5p, which leads to elevated integrin α9 (ITGA9), promoting migration and adhesion. Our study suggests the CUL4B/miR-194-5p/ITGA9 axis as an important regulator for macrophage infiltration in diabetic kidneys.

Effect of Infarct Location and Size on Left Atrial Function: A Cardiovascular Magnetic Resonance Feature Tracking Study.

Background: LA function has been recognized as a significant prognostic marker in many cardiovascular diseases. Cardiovascular magnetic resonance feature tracking (CMR-FT) represents a promising technique for left atrial function evaluation. The size and location of myocardial infarction are important factors in the cause of adverse left ventricular remodeling, but the effect on the left atriam is unclear. Purpose: to investigate the effect of location and size of previous myocardial infarction (MI) on LA function using CMR-FT. Study type: retrospective. Population: patients formerly diagnosed with anterior MI (n = 42) or non-anterior MI (n = 40) and healthy controls (n = 47). Field Strength/Sequence: a 3.0T MR, Steady state free precession (SSFP), Phase-sensitive inversion recovery (PSIR). Assessment: infarct location and size were assigned and quantified by late-gadolinium enhancement (LGE) imaging. LA performance was analyzed using CMR-FT in 2- and 4-chamber cine images, including LA reservoir, conduit and booster pump function. Statistics: descriptive statistics, ANOVA with post Bonferroni correction, Kruskal−Wallis H, Spearman's correlation, intraclass correlation coefficient. Results: Anterior MI patients had impaired LA reservoir function (LATEF, εs, SRs), conduit function (LAPEF, εe, SRs) and booster pump function (LAAEF, εa) compared with controls (p < 0.05). Non-anterior MI patients had impaired LA strain (εs, εe, εa; p < 0.05) but preserved LAEFs (p > 0.05). After adjusting the area of MI, there was no significant difference in the LA morphology and function between the anterior and non-anterior wall groups. Stratification analysis by MI size revealed that LA volumes and LAEFs were unchanged in patients with MI size ≤ 15% compared with controls (p > 0.05); only εs and εe were decreased (p < 0.05). Increased LAVIpre-a, LAVImin and decreased LATEF, and LAAEF were found in patients with MI size > 15% compared with the MI size ≤ 15% group (p < 0.05). LVSVI, εs and MI size were significant correlated with LAVI pre-a in multiple stepwise regression analysis. Data conclusions: The location of myocardial infarction is not a major factor affecting the morphology and function of the left atrium. Patients with MI size > 15% experience more pronounced post-infarction LA remodeling and dysfunction than MI size ≤ 15% patients.

Compound Mutations of the COL4A3 including a Novel Allele Identified in a Patient with Alport Syndrome.

Alport syndrome (AS) is a hereditary nephropathy which is characterized by molecular abnormalities in collagen IV. Here, we report compound mutations of the COL4A3 gene including a novel allele identified in a patient with Alport syndrome. The patient was a 25-year-old Chinese woman. She has a history of proteinuria and hematuria with cleft lip and palate. The pathologic results were consistent with Alport syndrome. The patient received ACEI treatment but did not respond well to the treatment. Sequencing results revealed that the patient carried two heterozygous mutations in the COL4A3 gene, including a known mutation (c.4243G>C, p.G1415R), which was inherited from her father, and a previously undescribed allele (c.4216G>A, p.G1406R) inherited from her mother. To date, at least 294 different variants of COL4A3 have been reported according to the Human Gene Mutation Database (HGMD). Identification of c.4216G>A as a new AS-related mutation may contribute to both genetic diagnosis of AS and further functional study of COL4A3.

Quantification of plaque characteristics detected by dual source computed tomography angiography to predict myocardial ischemia as assessed by single photon emission computed tomography myocardial perfusion imaging.

BACKGROUND: We aim to evaluate the relationship between quantitative plaque characteristics detected by dual-source computed tomography angiography (DSCTA) and myocardial ischemia as assessed by single photon emission computed tomography myocardial perfusion imaging (SPECT-MPI). METHODS: In this study, 460 consecutive patients with suspected coronary artery disease (CAD) underwent DSCTA and stress/rest SPECT-MPI, and 179 patients with coronary artery plaques were quantitatively analyzed. Quantitative coronary artery plaque measurements including total plaque volume, the volume of non-calcified plaque, calcified plaque volume, low-density noncalcified plaque volume, total plaque burden, calcified plaque burden, non-calcified plaque burden, low-density non-calcified plaque (LDNCP) burden, remodeling index, plaque length, maximum diameter stenosis were provided by the automated software (Release 5.6.5, Circle Cardiovascular Imaging, Canada). Univariate and multivariate logistic regression analysis was performed to assess the correlation between quantitative plaque characteristics and myocardial ischemia to determine if plaque characteristics were independent of clinical risk factors and significant CAD. RESULTS: One hundred and seventy-nine patients (65% males) with suspected-CAD, undergoing DSCTA and stress/rest SPECT-MPI and single vessel ischemia were considered. There were significant correlations between quantitative assessment of plaque features and myocardial ischemia with details as follow: total plaque volume [25.2 (17.8-37.8) vs. 15.6 (10.3-24.9) mm3, P<0.001], calcified plaque volume (1.6±7.1 vs. 2.3±6.4 mm3, P=0.019), non-calcified plaque volume [23.6 (16.6-35.9) vs. 14.6 (10.3-22.8) mm3, P<0.001)], LDNCP volume [4.9 (2.1-8.2) vs. 2.2 (1.0-5.5) mm3, P=0.003], total plaque burden (47.6%±17.1% vs. 36.2%±17.3%, P=0.002), calcified plaque burden (1.5%±5.5% vs. 2.9%±6.9%, P=0.014), non-calcified plaque burden (46.1%±18.8% vs. 33.3%±16.4%, P=0.001), LDNCP burden [12.3% (6.4-17.7) vs. 3.3% (1.6-5.3), P<0.001], remodeling index [1.2 (1.1-1.4) vs. 1.0 (1.1-1.2), P<0.001], plaque length [4.0 (3.2-6.1) vs. 3.3 (2.8-3.8) mm, P=0.009], maximum diameter stenosis [18.1% (10.0-52.9) vs. 12.9% (6.5-18.5), P=0.011]. In a multivariate analysis, low-density noncalcified plaque burden (OR 1.33; 95% CI, 1.16-1.53, P<0.001) remained a significant predictor of myocardial ischemia after adjusting for stenosis ≥50% and gender. The area under curve (AUC) of the model containing LDNCP burden, stenosis ≥50% and gender was 0.875 (95% CI, 0.812-0.938), which was significantly better than the model with stenosis ≥50% and gender (AUC 0.729; 95% CI, 0.633-0.825). CONCLUSIONS: Quantitative plaque characteristics detected by DSCTA are independently correlated with the incidence of myocardial ischemia by SPECT-MPI in patients with suspected CAD.

lncRNA CADM1-AS1 inhibits cell-cycle progression and invasion via PTEN/AKT/GSK-3ß axis in hepatocellular carcinoma.

Purpose: CADM1-AS1 (cell adhesion molecule 1 antisense RNA 1, long non-coding RNA), was firstly characterized in renal clear cell carcinoma, and exhibits a tumor suppressor role. However, its clinical relevance and exact effects in hepatocellular carcinoma (HCC) remain unknown. Therefore, in this study, we aimed to assess the clinical significance and function of CADM1-AS1 in HCC. Methods: We detected CADM1-AS1 expression in liver cancer tissue samples and cell lines, and analyzed the association between CADM1-AS1 expression and clinical parameters in 90 liver cancer patients. Moreover, we conducted gain-of-function and loss-of-function studies in liver cancer cell to explore the biological function and molecular mechanism of CADM1-AS1. Results: CADM1-AS1 expression was reduced in HCC. Clinical data showed that this downregulation was associated with advanced tumor stage, high TNM stage and reduced survival in HCC patients. CADM1-AS1 overexpression inhibited HCC cells proliferation, migration and invasion, while inducing G0/G1 phase arrest. Meanwhile, we revealed that CADM1-AS1 inhibited the phosphorylation of AKT and GSK-3ß. Furthermore, our study showed that CADM1-AS1 decreased the cell cycle associated proteins expression of cyclinD, cyclinE, CDK2 CDK4, CDK6, and enhanced the levels of p15, p21 and p27. More importantly, SC79, a specific activator for AKT;, apparently attenuated the effects of CADM1-AS1 on above cell-cycle associated proteins, confirming that CADM1-AS1 inhibited cell cycles through the AKT signaling pathway. And we also found the CADM1-AS1 has antitumor effect in vivo by a xenograft HCC mouse model. In conclusion, the present findings show that the CADM1-AS1 inhibits proliferation of HCC by inhibiting AKT/GSK-3ß signaling pathway, then upregulate p15, p21, p27 expression and downregulate cyclin, CDK expression to inhibit the G0/G1 to S phase transition both in vitro and in vivo. Conclusion: CADM1-AS1 functions as a tumor-suppressive lncRNA. This study reveals a molecular pathway involving PTEN/AKT/GSK-3ß which regulates HCC cell-cycle progression.

Lung nodules assessment in ultra-low-dose CT with iterative reconstruction compared to conventional dose CT.

BACKGROUND: To retrospectively assess whether the low-voltage lung CT scan coupled with iterative reconstruction algorithms can be an optimal scanning method for measuring the size and density of lung nodules in cancer patients. METHODS: Eighty two cancer patients receiving both chest scan with low-voltage (80 kV) and abdomen CT scan with standard voltage (120 kV) were enrolled in this study. Lung nodules were measured manually and semi-automatically by two different computer-aided diagnosis (CAD) systems. The nodules were then divided into large-, medium- and small-size groups based on their largest diameter. Additionally, the nodules were categorized into three different groups according to their density: calcified, solid and partial-solid nodules. The 3D volumes, average diameter and CT value of lung nodules were measured using the two CAD semi-automated systems, and the CT values were compared with regards to the different tube voltages. Furthermore, the accuracy and reliability of CAD systems were validated in the large nodules. RESULTS: The scores of subjective evaluation indicated that the quality of lung nodule images yielded optimal clinical diagnostic value for both 80 kV (2.35±0.054) and 120 kV (2.51±0.053) scanning methods, with a strong inter-observer consistency (Kappa =0.848 and 0.829, respectively). Intraclass correlation coefficient (ICC) and Bland-Altman plot revealed that two CAD systems produced the consistent results. Mean CT values of large nodules (n=18) were significantly different between 80 and 120 kV (-28.11±47.39 vs. -39.61±43.32 HU, P<0.05). Notably, the CT value of 80 kV was 33.96% higher than that of 120 kV. Moreover, the volumes of 66 solid lung nodules demonstrated a statistically significant difference (1.68%) between 80 kV group (740.89±156.97 mm3) and 120 kV group (753.48±157.92 mm3, P<0.05). Furthermore, significant differences were observed in the CT values of large nodules between 80 and 120 kV groups (25.64±12.67 vs. 13.89±9.78 HU, P<0.05), but not the maximum diameters (12.08±1.56 vs. 12.13±1.56 mm, P>0.05). CONCLUSIONS: Our study suggests that detection of lung nodules with ultra-low-dose CT can yield an excellent image quality and optimal diagnostic values as compared to the standard dose CT. Therefore, CT scan with low voltage of 80 kV CT scan can be leveraged to improve the diagnosis and surveillance of lung nodules measured less than 30 mm in diameter. Further investigation with a larger sample size is warranted to confirm our findings, particularly the increased CT values of large nodules and the greater volume of solid nodules after exposure to low-dose CT scan.

Control of resonant weak-light solitons via a periodic modulated control field.

We investigate propagation and control of weak-light spatial solitons in a resonant three-level atomic system with a periodic modulated control field. It is shown that the periodic modulation acts like periodic potential which resists the propagation of the soliton in transverse direction. The soliton could be trapped by the periodic potential in the input channel. When the modulation is canceled, the soliton propagates in its initial incident direction. The periodic modulation of control field could be used to control the propagation of the weak-light probe soliton. Due to the good localization efficiency of the periodic potential, an excellent switching is realized for the probe soliton. These properties may have potential applications in all-optical switching, optical information processing and other fields.

Tunneling-induced large cross-phase modulation in an asymmetric quantum well.

We propose an asymmetric double AlGaAs/GaAs quantum well structure with a common continuum to generate a large cross-phase modulation (XPM). It is found, owing to resonant tunneling, that a large XPM can be achieved with vanishing linear and two-photon absorptions.