Multi-organ Segmentation via Co-training Weight-averaged Models from Few-organ Datasets

Multi-organ segmentation has extensive applications in many clinical applications. To segment multiple organs of interest, it is generally quite difficult to collect full annotations of all the organs on the same images, as some medical centers might only annotate a portion of the organs due to their own clinical practice. In most scenarios, one might obtain annotations of a single or a few organs from one training set, and obtain annotations of the the other organs from another set of training images. Existing approaches mostly train and deploy a single model for each subset of organs, which are memory intensive and also time inefficient. In this paper, we propose to co-train weight-averaged models for learning a unified multi-organ segmentation network from few-organ datasets. We collaboratively train two networks and let the coupled networks teach each other on un-annotated organs. To alleviate the noisy teaching supervisions between the networks, the weighted-averaged models are adopted to produce more reliable soft labels. In addition, a novel region mask is utilized to selectively apply the consistent constraint on the un-annotated organ regions that require collaborative teaching, which further boosts the performance. Extensive experiments on three public available single-organ datasets LiTS, KiTS, Pancreas and manually-constructed single-organ datasets from MOBA show that our method can better utilize the few-organ datasets and achieves superior performance with less inference computational cost.Comment: Accepted by MICCAI 202

Mechanical Impact Noise Analysis of Rotary Compressor

In the noise and vibration test of 8HP rotary compressor, the peak value of noise and vibration is especially high at frequency range between 600~1000Hz. The sound pressure level (SPL) exceeds the enterprise criterions and the sound quality is so tough that persons cannot bear such annoying noise. Two experiments, pressure pulsation above/ below compressor motor and mechanical impacts of compressor pump-rotor unit, are particularly carried out in order to identify the noise sources. The test results confirm that the axial up-down movement of pump-rotor unit is the primary reason, causing the abnormal noise and vibration. Several measures, including partially cutting the circumferential edge of the stator and increase the height differential between rotor and stator, have been taken in order to reduce pressure pulsation above/below motor and restrain the axial movement of shaft-rotor unit. With these measures, the noise problem of 8HP rotary compressor has been solved successfully. Finally the sound pressure level decreases about 4dB and the sound quality is comfortable and good to hear.

The role of EGFR double minutes in modulating the response of malignant gliomas to radiotherapy.

EGFR amplification in cells having double minute chromosomes (DM) is commonly found in glioblastoma multiforme (GBM); however, how much it contributes to the current failure to treat GBM successfully is unknown. We studied two syngeneic primary cultures derived from a GBM with and without cells carrying DM, for their differential molecular and metabolic profiles, in vivo growth patterns, and responses to irradiation (IR). Each cell line has a distinct molecular profile consistent with an invasive "go" (with DM) or angiogenic "grow" phenotype (without DM) demonstrated in vitro and in intracranial xenograft models. Cells with DM were relatively radio-resistant and used higher glycolytic respiration and lower oxidative phosphorylation in comparison to cells without them. The DM-containing cell was able to restore tumor heterogeneity by mis-segregation of the DM-chromosomes, giving rise to cell subpopulations without them. As a response to IR, DM-containing cells switched their respiration from glycolic metabolism to oxidative phosphorylation and shifted molecular profiles towards that of cells without DM. Irradiated cells with DM showed the capacity to alter their extracellular microenvironment to not only promote invasiveness of the surrounding cells, regardless of DM status, but also to create a pro-angiogenic tumor microenvironment. IR of cells without DM was found primarily to increase extracellular MMP2 activity. Overall, our data suggest that the DM-containing cells of GBM are responsible for tumor recurrence due to their high invasiveness and radio-resistance and the mis-segregation of their DM chromosomes, to give rise to fast-growing cells lacking DM chromosomes

A primary Rosai-Dorfman-Destombes disease of the scalp: case report and literature review

BackgroundRosai-Dorfman-Destombes disease (RDD) was first described in 1965 as a benign histiocytic proliferative disorder of unknown cause. Cases of RDD limited to cutaneous tissue have been reported over the past few decades, but single cutaneous RDD of the scalp is rare.Case presentationWe report a 31-year-old male with a lump on the parietal scalp without extranodal lesion lasting 1 month with gradual enlargement. The surgical incision ruptured with purulent after the first resection. Then the patient was treated with plastic surgery after disinfection and antibiotic treatment. Finally, he recovered well and discharged after 20 days.ConclusionsRDD of the scalp is rare. Surgical incision can cure the lesion but it may become infected because of increased lymphocytic infiltration. Early diagnosis and differential diagnosis of RDD are necessary. For treatment, individualized therapy is critical to patient prognosis

Synergistic structural and functional alterations in the medial prefrontal cortex of patients with high-grade gliomas infiltrating the thalamus and the basal ganglia

BackgroundHigh-grade gliomas (HGGs) are characterized by a high degree of tissue invasion and uncontrolled cell proliferation, inevitably damaging the thalamus and the basal ganglia. The thalamus exhibits a high level of structural and functional connectivity with the default mode network (DMN). The present study investigated the structural and functional compensation within the DMN in HGGs invading the thalamus along with the basal ganglia (HITBG).MethodsA total of 32 and 22 healthy controls were enrolled, and their demographics and neurocognition (digit span test, DST) were assessed. Of the 32 patients, 18 patients were involved only on the left side, while 15 of them were involved on the right side. This study assessed the amplitude of low-frequency fluctuation (ALFF), regional homogeneity (ReHo), gray matter (GM) volume, and functional connectivity (FC) within the DMN and compared these measures between patients with left and right HITBG and healthy controls (HCs).ResultThe medial prefrontal cortex (mPFC) region existed in synchrony with the significant increase in ALFF and GM volume in patients with left and right HITBG compared with HCs. In addition, patients with left HITBG exhibited elevated ReHo and GM precuneus volumes, which did not overlap with the findings in patients with right HITBG. The patients with left and right HITBG showed decreased GM volume in the contralateral hippocampus without any functional variation. However, no significant difference in FC values was observed in the regions within the DMN. Additionally, the DST scores were significantly lower in patients with HITBG, but there was no significant correlation with functional or GM volume measurements.ConclusionThe observed pattern of synchrony between structure and function was present in the neuroplasticity of the mPFC and the precuneus. However, patients with HITBG may have a limited capacity to affect the connectivity within the regions of the DMN. Furthermore, the contralateral hippocampus in patients with HITBG exhibited atrophy. Thus, preventing damage to these regions may potentially delay the progression of neurological function impairment in patients with HGG

The adenosine A2A receptor antagonist KW6002 distinctly regulates retinal ganglion cell morphology during postnatal development and neonatal inflammation

Adenosine A2A receptors (A2ARs) appear early in the retina during postnatal development, but the roles of the A2ARs in the morphogenesis of distinct types of retinal ganglion cells (RGCs) during postnatal development and neonatal inflammatory response remain undetermined. As the RGCs are rather heterogeneous in morphology and functions in the retina, here we resorted to the Thy1-YFPH transgenic mice and three-dimensional (3D) neuron reconstruction to investigate how A2ARs regulate the morphogenesis of three morphologically distinct types of RGCs (namely Type I, II, III) during postnatal development and neonatal inflammation. We found that the A2AR antagonist KW6002 did not change the proportion of the three RGC types during retinal development, but exerted a bidirectional effect on dendritic complexity of Type I and III RGCs and cell type-specifically altered their morphologies with decreased dendrite density of Type I, decreased the dendritic field area of Type II and III, increased dendrite density of Type III RGCs. Moreover, under neonatal inflammation condition, KW6002 specifically increased the proportion of Type I RGCs with enhanced the dendrite surface area and volume and the proportion of Type II RGCs with enlarged the soma area and perimeter. Thus, A2ARs exert distinct control of RGC morphologies to cell type-specifically fine-tune the RGC dendrites during normal development but to mainly suppress RGC soma and dendrite volume under neonatal inflammation

PAX6 suppression of glioma angiogenesis and the expression of vascular endothelial growth factor A

We reported that PAX6 suppresses glioblastoma cell growth in vivo and anchorage-independent growth without significant alteration of cell proliferation in vitro, suggesting that PAX6 may alter the tumor microenvironment. Because we found that PAX6 downregulates expression of the gene encoding vascular endothelial growth factor A (VEGFA) in glioma cells, we used a subcutaneous xenograft model to verify PAX6 suppression of VEGFA-induced angiogenesis based on CD31-immunostaining of endothelial cells. The results showed a significant reduction of VEGFA at the transcription level in PAX6-transfected cells in xenografts and PAX6 has a suppressive effect on the microvascular amplification typically seen in glioblastoma. We showed that PAX6 suppression of VEGFA expression requires its DNA binding-domain. The C-terminal truncation mutant of PAX6, however, did not show the dominant negative function in regulating VEGFA expression that it showed previously in regulating MMP2 expression. In the glioma cell line U251HF, we further determined that blocking the PI3K/Akt signaling pathway with either adenoviral-mediated PTEN expression or LY294002 enhanced PAX6-mediated suppression of VEGFA in an additive manner; thus, PAX6-mediated suppression of VEGFA is not via the canonical pathway through HIF1A. These two VEGFA-regulatory pathways can also be similarly modulated in another malignant glioma cell line, U87, but not in LN229 where the basal VEGFA level is low and PTEN is wild-type. PAX6 suppression of VEGFA appears to be blocked in LN229. In conclusion, our data showed that PAX6 can initiate in glioma cells a new signaling pathway independent of PI3K/Akt-HIF1A signaling to suppress VEGFA expression

RNA Helicase DDX17 Inhibits Hepatitis B Virus Replication by Blocking Viral Pregenomic RNA Encapsidation

DDX17 is a member of the DEAD-box helicase family proteins involved in cellular RNA folding, splicing, and translation. It has been reported that DDX17 serves as a cofactor of host zinc finger antiviral protein (ZAP)-mediated retroviral RNA degradation and exerts direct antiviral function against Raft Valley fever virus through binding to specific stem-loop structures of viral RNA. Intriguingly, we have previously shown that ZAP inhibits hepatitis B virus (HBV) replication through promoting viral RNA decay, and the ZAP-responsive element (ZRE) of HBV pregenomic RNA (pgRNA) contains a stem-loop structure, specifically epsilon, which serves as the packaging signal for pgRNA encapsidation. In this study, we demonstrated that the endogenous DDX17 is constitutively expressed in human hepatocyte-derived cells but dispensable for ZAP-mediated HBV RNA degradation. However, DDX17 was found to inhibit HBV replication primarily by reducing the level of cytoplasmic encapsidated pgRNA in a helicase-dependent manner. Immunofluorescence assay revealed that DDX17 could gain access to cytoplasm from nucleus in the presence of HBV RNA. In addition, RNA immunoprecipitation and electrophoretic mobility shift assays demonstrated that the enzymatically active DDX17 competes with HBV polymerase to bind to pgRNA at the 5' epsilon motif. In summary, our study suggests that DDX17 serves as an intrinsic host restriction factor against HBV through interfering with pgRNA encapsidation. IMPORTANCE Hepatitis B virus (HBV) chronic infection, a long-studied but yet incurable disease, remains a major public health concern worldwide. Given that HBV replication cycle highly depends on host factors, deepening our understanding of the host-virus interaction is thus of great significance in the journey of finding a cure. In eukaryotic cells, RNA helicases of the DEAD box family are highly conserved enzymes involved in diverse processes of cellular RNA metabolism. Emerging data have shown that DDX17, a typical member of the DEAD box family, functions as an antiviral factor through interacting with viral RNA. In this study, we, for the first time, demonstrate that DDX17 inhibits HBV through blocking the formation of viral replication complex, which not only broadens the antiviral spectrum of DDX17 but also provides new insight into the molecular mechanism of DDX17-mediated virus-host interaction

Healthy lifestyle and life expectancy free of major chronic diseases at age 40 in Chinese population: a prospective cohort study

Background: A healthy lifestyle has been associated with a longer life expectancy (LE). However, whether it also helps achieve gains in LE free of major non-communicable diseases (NCDs) and its share of total LE in Chinese adults remains unknown. Methods: We used data from China Kadoorie Biobank (CKB) of 451,233 adults aged 30-79 free of heart disease, stroke, cancer, chronic obstructive pulmonary disease (COPD), and asthma at baseline. Low-risk lifestyle factors included never smoking or quitting for reasons other than illness, no excessive alcohol use, being physically active, healthy eating habits, and healthy body shape. We built multistate life tables for individuals with different risk levels of lifestyle factors to calculate LE with and without diseases (cardiovascular diseases [CVDs], cancer, chronic respiratory diseases [CRDs, including COPD and asthma]) at age 40. For life table calculation, we used prevalence of lifestyle factors, transition rates, and hazard ratios (HRs) for three transitions (disease-free to disease onset, disease-free to death, and presence of disease to all-cause mortality). Findings: During a median follow-up of 11.1 years, we documented 111,002 new CVD cases, 24,635 cancer cases, 12,506 CRD cases, and 34,740 deaths. The adjusted HRs (95% confidence intervals [CIs]) of men adopting all five versus 0-1 low-risk factors was 0.56 (0.50, 0.63), 0.40 (0.20, 0.80), and 0.64 (0.50, 0.83) for baseline to disease, baseline to death, and disease to death, respectively; the corresponding values for women were 0.69 (0.64, 0.75), 0.57 (0.34, 0.94), and 0.57 (0.47, 0.69). The LE free of the three NCDs (95%CI) at age 40 for individuals with 0-1 low-risk factor was on average 23.9 (23.2, 24.6) years for men and 24.2 (23.5, 24.9) years for women. For individuals adopting all five low-risk factors, it was 30.2 (28.8, 31.6) years for men and 28.4 (27.2, 29.6) years for women, with an increase of 6.3 (5.1, 7.5) years (men) and 4.2 (3.6, 5.4) years (women). Correspondingly, the proportion of LE free of the three NCDs to total LE increased from 73.1% to 76.3% for men and from 67.6% to 68.4% for women. Interpretation: Our findings suggest that promoting healthy lifestyles through public health interventions could be associated with increased LE free of major NCDs and 'relative compression of morbidity' in the Chinese population

Electronic health record–based absolute risk prediction model for esophageal cancer in the Chinese population: model development and external validation

Background: China has the largest burden of esophageal cancer (EC). Prediction models can be used to identify high-risk individuals for intensive lifestyle interventions and endoscopy screening. However, the current prediction models are limited by small sample size and a lack of external validation, and none of them can be embedded into the booming electronic health records (EHRs) in China. Objective: This study aims to develop and validate absolute risk prediction models for EC in the Chinese population. In particular, we assessed whether models that contain only EHR-available predictors performed well. Methods: A prospective cohort recruiting 510,145 participants free of cancer from both high EC-risk and low EC-risk areas in China was used to develop EC models. Another prospective cohort of 18,441 participants was used for validation. A flexible parametric model was used to develop a 10-year absolute risk model by considering the competing risks (full model). The full model was then abbreviated by keeping only EHR-available predictors. We internally and externally validated the models by using the area under the receiver operating characteristic curve (AUC) and calibration plots and compared them based on classification measures. Results: During a median of 11.1 years of follow-up, we observed 2550 EC incident cases. The models consisted of age, sex, regional EC-risk level (high-risk areas: 2 study regions; low-risk areas: 8 regions), education, family history of cancer (simple model), smoking, alcohol use, BMI (intermediate model), physical activity, hot tea consumption, and fresh fruit consumption (full model). The performance was only slightly compromised after the abbreviation. The simple and intermediate models showed good calibration and excellent discriminating ability with AUCs (95% CIs) of 0.822 (0.783-0.861) and 0.830 (0.792-0.867) in the external validation and 0.871 (0.858-0.884) and 0.879 (0.867-0.892) in the internal validation, respectively. Conclusions: Three nested 10-year EC absolute risk prediction models for Chinese adults aged 30-79 years were developed and validated, which may be particularly useful for populations in low EC-risk areas. Even the simple model with only 5 predictors available from EHRs had excellent discrimination and good calibration, indicating its potential for broader use in tailored EC prevention. The simple and intermediate models have the potential to be widely used for both primary and secondary prevention of EC