Nutrient intake and risk of multimorbidity: a prospective cohort study of 25,389 women.

BACKGROUND: Multimorbidity is becoming an increasingly serious public health challenge in the aging population. The impact of nutrients on multimorbidity remains to be determined and was explored using data from a UK cohort study. METHOD: Our research analysis is mainly based on the data collected by the United Kingdom Women's Cohort Study (UKWCS), which recruited 35,372 women aged 35-69 years at baseline (1995 to 1998), aiming to explore potential associations between diet and chronic diseases. Daily intakes of energy and nutrients were estimated using a validated 217-item food frequency questionnaire at recruitment. Multimorbidity was assessed using the Charlson comorbidity index (CCI) through electronic linkages to Hospital Episode Statistics up to March 2019. Cox's proportional hazards models were used to estimate associations between daily intakes of nutrients and risk of multimorbidity. Those associations were also analyzed in multinomial logistic regression as a sensitivity analysis. In addition, a stratified analysis was conducted with age 60 as the cutoff point. RESULTS: Among the 25,389 participants, 7,799 subjects (30.7%) were confirmed with multimorbidity over a median follow-up of 22 years. Compared with the lowest quintile, the highest quintile of daily intakes of energy and protein were associated with 8% and 12% increased risk of multimorbidity respectively (HR 1.08 (95% CI 1.01, 1.16), p-linearity = 0.022 for energy; 1.12 (1.04, 1.21), p-linearity = 0.003 for protein). Higher quintiles of daily intakes of vitamin C and iron had a slightly lowered risk of multimorbidity, compared to the lowest quintile. A significantly higher risk of multimorbidity was found to be linearly associated with higher intake quintiles of vitamin B12 and vitamin D (p-linearity = 0.001 and 0.002, respectively) in Cox models, which became insignificant in multinomial logistic regression. There was some evidence of effect modification by age in intakes of iron and vitamin B1 associated with the risk of multimorbidity (p-interaction = 0.006 and 0.025, respectively). CONCLUSIONS: Our findings highlight a link between nutrient intake and multimorbidity risk. However, there is uncertainty in our results, and more research is needed before definite conclusions can be reached.

Potential of PAQosome as a therapeutic target for hepatic fibrosis.

BACKGROUND AND AIM: The condition of hepatic fibrosis is hazardous. Therefore, it is vital that we investigate the mechanism of hepatic fibrosis to provide new targets for treatment. METHODS: Preliminary screening and research was carried out based on our prior results and our speculated role of the particle with quaternary structure arrangement (PAQosome) in hepatic fibrosis. The experiments were conducted using LX-2 or HepG2 cell lines by western blotting, quantitative real-time polymerase chain reaction, luciferase assays, and co-immunoprecipitation and were further validated in the Gene Expression Omnibus (GEO) database. RESULTS: We screened and proved that several subunits of the PAQosome regulate the development of liver fibrosis, including the asparagine synthetase domain-containing 1 upstream open reading frame (ASDURF), prefoldin subunit 4 (PFDN4), prefoldin subunit 5 (PFDN5), unconventional prefoldin RNA polymerase II subunit 5 interactor (URI1), and ubiquitously expressed prefoldin-like chaperone (UXT). ASDURF promotes hepatic fibrosis through the transforming growth factor-ß1 (TGFß1)/Sekelsky mothers against decapentaplegic homologue 3 (Smad3) and NF-κB signaling pathways. ASDURF regulates the expression of asparagine synthetase domain-containing 1 (ASNSD1). PFDN4, PFDN5, URI1, and UXT regulate cell proliferation through the PI3K/AKT pathway, and thus regulate liver fibrosis. A hepatic fibrosis score ≥ F2 was selected as the diagnostic criteria for hepatic fibrosis in the GSE96971 database. The area under the receiver operating characteristic curve of PFDN4, PFDN5, UXT, and ASNSD1 were 0.862 (confidence interval [CI]: 0.6588-1.000), 0.538 (CI: 0.224-0.853), 0.708 (CI: 0.449-0.966), and 0.831 (CI: 0.638-1.000), respectively. CONCLUSIONS: These findings demonstrate that the PAQosome is a brand new target for hepatic fibrosis therapy.

Deficiency of circ_0103809 Attenuates Non-small Cell Lung Cancer Malignant Progression by Controlling miR-153-3p/HDAC1 Network.

Circular RNAs are vital players in tumorigenesis. We held the purpose to investigate the role and mechanism of circ_0103809 in non-small cell lung cancer (NSCLC). The expressions of circ_0103809, miR-153-3p and HDAC1 mRNA were determined using quantitative real-time PCR assay, and HDAC1 protein was quantified using western blot analysis. MTT, EdU, flow cytometry, tube-formation, wound healing and tube-formation assays were conducted for functional analysis. The predicted relationship among circ_0103809, miR-153-3p and HDAC1 was ascertained using dual-luciferase analysis, RIP assay and pull-down analysis. Animal models were further constructed to realize circ_0103809's role in vivo. Circ_0103809 was upregulated NSCLC specimens, cells and serum-derived exosomes. Serum exosomal circ_0103809 had the potency to be a diagnostic biomarker for NSCLC. Circ_0103809 silencing inhibited NSCLC cell growth, metastasis and angiogenesis and triggered cell cycle arrest and apoptosis. Circ_0103809 deficiency also suppressed the growth of transplanted tumors. Circ_0103809 acted as the miR-153-3p sponge, and the biological effects of circ_0103809 knockdown were relieved by miR-153-3p inhibition. HDAC1 was directly targeted by miR-153-3p, and miR-153-3p enrichment inhibited NSCLC cell malignant phenotypes by sequestering HDAC1. Circ_0103809 knockdown repressed NSCLC malignant progression partly by regulating miR-153-3p/HDAC1 signaling.

Calcitriol attenuates liver fibrosis through hepatitis C virus nonstructural protein 3-transactivated protein 1-mediated TGF ß1/Smad3 and NF-κB signaling pathways.

BACKGROUND: Hepatic fibrosis is a serious condition, and the development of hepatic fibrosis can lead to a series of complications. However, the pathogenesis of hepatic fibrosis remains unclear, and effective therapy options are still lacking. Our group identified hepatitis C virus nonstructural protein 3-transactivated protein 1 (NS3TP1) by suppressive subtractive hybridization and bioinformatics analysis, but its role in diseases including hepatic fibrosis remains undefined. Therefore, additional studies on the function of NS3TP1 in hepatic fibrosis are urgently needed to provide new targets for treatment. AIM: To elucidate the mechanism of NS3TP1 in hepatic fibrosis and the regulatory effects of calcitriol on NS3TP1. METHODS: Twenty-four male C57BL/6 mice were randomized and separated into three groups, comprising the normal, fibrosis, and calcitriol treatment groups, and liver fibrosis was modeled by carbon tetrachloride (CCl4). To evaluate the level of hepatic fibrosis in every group, serological and pathological examinations of the liver were conducted. TGF-ß1 was administered to boost the in vitro cultivation of LX-2 cells. NS3TP1, α-smooth muscle actin (α-SMA), collagen I, and collagen III in every group were examined using a Western blot and real-time quantitative polymerase chain reaction. The activity of the transforming growth factor beta 1 (TGFß1)/Smad3 and NF-κB signaling pathways in each group of cells transfected with pcDNA-NS3TP1 or siRNA-NS3TP1 was detected. The statistical analysis of the data was performed using the Student's t test. RESULTS: NS3TP1 promoted the activation, proliferation, and differentiation of hepatic stellate cells (HSCs) and enhanced hepatic fibrosis via the TGFß1/Smad3 and NF-κB signaling pathways, as evidenced by the presence of α-SMA, collagen I, collagen III, p-smad3, and p-p65 in LX-2 cells, which were upregulated after NS3TP1 overexpression and downregulated after NS3TP1 interference. The proliferation of HSCs was lowered after NS3TP1 interference and elevated after NS3TP1 overexpression, as shown by the luciferase assay. NS3TP1 inhibited the apoptosis of HSCs. Moreover, both Smad3 and p65 could bind to NS3TP1, and p65 increased the promoter activity of NS3TP1, while NS3TP1 increased the promoter activity of TGFß1 receptor I, as indicated by coimmunoprecipitation and luciferase assay results. Both in vivo and in vitro, treatment with calcitriol dramatically reduced the expression of NS3TP1. Calcitriol therapy-controlled HSCs activation, proliferation, and differentiation and substantially suppressed CCl4-induced hepatic fibrosis in mice. Furthermore, calcitriol modulated the activities of the above signaling pathways via downregulation of NS3TP1. CONCLUSION: Our results suggest that calcitriol may be employed as an adjuvant therapy for hepatic fibrosis and that NS3TP1 is a unique, prospective therapeutic target in hepatic fibrosis.

Organic Passivation of Deep Defects in Cu(In,Ga)Se2 Film for Geometry-Simplified Compound Solar Cells.

Diverse defects in copper indium gallium diselenide solar cells cause nonradiative recombination losses and impair device performance. Here, an organic passivation scheme for surface and grain boundary defects is reported, which employs an organic passivation agent to infiltrate the copper indium gallium diselenide thin films. A transparent conductive passivating (TCP) film is then developed by incorporating metal nanowires into the organic polymer and used in solar cells. The TCP films have a transmittance of more than 90% in the visible and nearinfrared spectra and a sheet resistance of ~10.5 Ω/sq. This leads to improvements in the open-circuit voltage and the efficiency of the organic passivated solar cells compared with control cells and paves the way for novel approaches to copper indium gallium diselenide defect passivation and possibly other compound solar cells.

Multi-Carrier Generation in Organic-Passivated Black Silicon Solar Cells with Industrially Feasible Processes.

The innate inverse Auger effect within bulk silicon can result in multiple carrier generation. Observation of this effect is reliant upon low high-energy photon reflectance and high-quality surface passivation. In the photovoltaics industry, metal-assisted chemical etching (MACE) to afford black silicon (b-Si) can provide a low high-energy photon reflectance. However, an industrially feasible and cheaper technology to conformally passivate the outer-shell defects of these nanowires is currently lacking. Here, a technology is introduced to infiltrate black silicon nanopores with a simple and vacuum-free organic passivation layer that affords millisecond-level minority carrier lifetimes and matches perfectly with existing solution-based processing of the MACE black silicon. Advancements such as the demonstration of an excellent passivation effect whilst also being low reflectance provide a new technological route for inverse Auger multiple carrier generation and an industrially feasible technical scheme for the development of the MACE b-Si solar cells.

Neurotoxicity of sanguinarine via inhibiting mitophagy and activating apoptosis in zebrafish and PC12 cells.

Sanguinarine, a plant-derived phytoalexin, displays various biological activities, such as insecticidal, antimicrobial, anti-inflammatory, anti-angiogenesis and antitumor effects. But its potential neurotoxicity and the underlying mechanisms has rarely been investigated. Therefore, we aimed to assess the neurotoxicity of sanguinarine using zebrafish model and PC12 cells in this study. The results showed that sanguinarine induced the reduction of the length of dopamine neurons and inhibited the blood vessel in the head area of the zebrafish. Further studies demonstrated that the behavioral phenotype of the larval zebrafish was changed by sanguinarine. In addition, there were more apoptotic cells in the larval zebrafish head area. The mRNA expression levels of ß-syn, th, pink1 and parkin, closely related to the nervous function, were changed after sanguinarine treatment. The in vitro studies show that notably increases of ROS and apoptosis levels in PC12 cells were observed after sanguinarine treatment. Moreover, the protein expression of Caspase3, Parp, Bax, Bcl2, α-Syn, Th, PINK1 and Parkin were also altered by sanguinarine. Our data indicated that the inhibition of mitophagy, ROS elevation and apoptosis were involved in the neurotoxicity of sanguinarine. These findings will be useful to understand the toxicity induced by sanguinarine.

The decline of HBV RNA associated with HBeAg seroconversion and double-negative HBV DNA and RNA in chronic hepatitis B patients who received entecavir therapy: a 10-year retrospective cohort study.

Background: Whether the decline of hepatitis B virus (HBV) RNA was associated with antiviral efficacy in chronic hepatitis B (CHB) patients receiving long-term nucleos(t)ide analogues (NAs) therapy remains unclear. We observed the levels of serum HBV RNA in CHB patients treated with entecavir (ETV) for 10 years and explored the clinical significance of HBV RNA during long-term antiviral treatment. Methods: A total of 33 hepatitis B surface antigen (HBsAg)-positive CHB patients treated with ETV for up to 10 years were recruited for this study. Liver function, HBsAg, hepatitis B envelope antigen (HBeAg), HBV DNA, and HBV RNA were measured at the baseline and each follow-up points. Antiviral efficacy was defined as negative HBV DNA (<20 IU/mL) and HBV RNA (<300 Copies/mL). Results: (I) Serum HBV DNA and HBV RNA declined with the duration of antiviral treatment over 10 years (P<0.001). (II) There were positive correlations between serum HBV DNA and HBV RNA at each follow-up point (r=0.62 and P<0.001 at baseline, r=0.77 and P<0.001 at week 24, r=0.71 and P<0.001 at week 48, r=0.81 and P<0.001 at week 96, r=0.60 and P<0.01 at year 5 and r=0.77 and P<0.001 at year 10). (III) HBeAg and HBsAg levels at baseline and 10th year after ETV treatment have significant difference (P<0.05 and P<0.01). (IV) The decline of HBV RNA after ETV treatment was associated with HBeAg seroconversion, the area under the ROC curves (AUROCs) of the declines of HBV RNA were 0.25 at the baseline, 0.62 at week 24, 0.78 at week 48 and 0.86 at week 96, respectively. (V) The decline of HBV RNA after ETV treatment was associated with antiviral efficacy, the AUROCs of the declines of HBV RNA were 0.33 at the baseline, 0.74 at week 24, 0.83 at week 48 and 0.86 at week 96, respectively. Conclusions: Serum HBV DNA and HBV RNA declined with the duration of antiviral treatment over 10 years. The decline of HBV RNA was associated with HBeAg seroconversion and antiviral efficacy in CHB patients receiving long-term ETV therapy, and the earliest prediction point was week 24.

SPP1 and CXCL9 Promote Non-alcoholic Steatohepatitis Progression Based on Bioinformatics Analysis and Experimental Studies.

Background and Aims: Non-alcoholic fatty liver disease (NAFLD) is a major chronic liver disease worldwide, and non-alcoholic steatohepatitis (NASH) is one of its pathological subtypes. The pathogenesis of NASH has not yet been fully elucidated. The purpose of this study was to identify the hub genes and pathways involved in NASH using bioinformatics methods. The hub genes were confirmed in human and animal models. Materials and Methods: Three Gene Expression Omnibus (GEO) datasets (GSE48452, GSE58979, and GSE151158) of NASH patients and healthy controls were included in the study. We used GEO2R to identify differentially expressed genes (DEGs) between NASH patients and healthy controls. Functional enrichment analyses were then performed to explore the potential functions and pathways of the DEGs. In all DEGs, only two genes were highly expressed in NASH patients throughout the three datasets; these two genes, SPP1 and CXCL9, were further studied. Serum and liver tissues from NASH patients and healthy controls were collected. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels were measured in NASH patients and healthy controls. Liver tissues were stained with hematoxylin and eosin. Immunohistochemical staining was used to evaluate the expression levels of the two genes in liver tissues. Male C57BL/6J mice were fed a methionine choline-deficient (MCD) diet for 8 weeks, after which serum ALT and AST levels were measured and liver tissues were stained. Results: SPP1 and CXCL9 were the hub genes detected in the three datasets. "Lipid metabolism," "inflammatory response," and "lymphocyte activation" were the most significant biological functions in GSE48452, GSE58979, and GSE151158, respectively. Kyoto Encyclopedia of Genes and Genomes pathway analysis showed that the toll-like receptor signaling pathway was significantly enriched in NASH patients. Serum ALT and AST levels were significantly increased in NASH patients compared to healthy controls. Liver tissues had more serious steatosis, hepatocyte ballooning degeneration, and lobular inflammatory infiltration, and the expression of SPP1 and CXCL9 in liver cells was significantly upregulated in NASH patients compared to healthy controls. MCD diet mice were consistent with NASH patients. Conclusion: SPP1 and CXCL9 may play important roles in NASH pathogenesis and could be potential therapeutic targets and biomarkers of NASH in the future. Further experimental studies are needed to confirm our results.

Cord blood metabolomics reveals gestational metabolic disorder associated with anti-thyroid peroxidase antibodies positivity.

BACKGROUND: Thyroid disease is one of the common endocrine disorders affecting the pregnant women, in which thyroid autoimmunity can alter the progress and the outcome of pregnancy. Women with euthyroid status but anti-thyroid peroxidase (anti-TPO) antibodies positivity before pregnancy are prone to subclinical gestational hypothyroidism. However, the connections between anti-TPO antibodies positivity and gestational hypothyroidism remain largely unknown. The aim of the present study is to investigate the differences of fetal metabolic profile at birth according to maternal anti-TPO status. METHODS: We performed 1H-NMR metabolomics on cord blood of a nested case control cohort of 22 pregnant women with matched thyroid hormone levels and demographic data, including 11 women with euthyroid status but anti-thyroid antibodies positivity (into the anti-TPO antibodies positivity group) and 11 matched women as controls with euthyroid status and negative anti-thyroid antibodies (into the control group). RESULTS: Distinct metabolic profiles were observed between the anti-TPO antibody positivity group and the nested control group, from which a total of 10 metabolites with between-group altered abundances were structurally identified. Five out of the 10 metabolites were up-regulated in the anti-TPO antibodies positivity group, including D-Glucose, L-Glutamine, 3-Hydroxybutyric acid, Myo-Inositol, Creatinine. The other 5 metabolites were down-regulated in the anti-TPO antibodies positivity group, including L-Leucine, L-Lysine, L-Glutamic acid, L-Tyrosine, and L-Phenylalanine. All the 10 metabolites have been previously reported to be correlated with hypothyroidism. Metabolite set enrichment analysis and pathway analysis suggested that amino acid metabolism pathways (especially the phenylalanine metabolism) were associated with anti-TPO antibodies positivity. CONCLUSION: The results of this study suggested that fetal metabolic disorder is correlated with anti-TPO antibodies positivity, representing by abundance alteration of hypothyroidism associated metabolites and the related disturbance of amino acid metabolism pathways.

Severe Vitamin D Deficiency Is Strongly Associated with Liver Dysfunction and Disease Severity in Hepatitis B Virus Related Cirrhosis and Liver Failure Patients.

Vitamin D deficiency is common in chronic liver diseases, it may increase the severity of the diseases. However, studies on the potential role of vitamin D in hepatitis B virus (HBV) related end stage liver disease are still limited. This study was performed to assess the prevalence of vitamin D deficiency in patients with different stages of chronic HBV infection and explore whether vitamin D deficiency can be established as an index of severity and prognosticator of disease progression. Serum 25(OH)D3 levels were measured in a cohort of 363 patients with chronic HBV infection. Biochemical parameters, the alpha fetoprotein level, HBV DNA load, hepatitis B surface antigen level, and hepatitis B early antigen level were tested. The mean 25(OH)D3 level was significantly lower in patients with chronic HBV-related liver disease than in healthy controls. Overall, 74.9% of patients had 25(OH)D3 deficiency. The 25(OH)D3 level was significantly positively correlated with the albumin level. In total, 77.6% (121/156) of patients with cirrhosis had vitamin D deficiency. The 25(OH)D3 level significantly decreased as the Child-Pugh classification increased in severity. The 25(OH)D3 level was negatively correlated with the model for end-stage liver disease (MELD) score and low 25(OH)D3 concentrations were significantly associated with high MELD score and mortality in patients with liver failure. Vitamin D deficiency is prevalent in patients with chronic HBV infection. Severe vitamin D deficiency is strongly related to liver dysfunction and disease severity in the cirrhosis and liver failure patients.

Hereditary Spherocytosis With Liver Transplantation After Cirrhosis: A Case Report.

The clinical manifestations of hereditary spherocytosis are similar to those of various hemolytic anemias, which causes hereditary spherocytosis to be difficult to diagnose clinically. In this case, we obtained the peripheral blood of a patient and family members, and through a whole exome test of the 6,297 genetic phenotypes confirmed by OMIM, we found a heterozygous nonsense mutation (c.4117C>T, P.Q1373X) in the SPTB gene. Combined with the patient's clinical data, the diagnosis was hereditary spherocytosis. Compared with the public population sequence database, the mutation was found to be unique. Through protein structure prediction analysis and literature studies, we found that the mutation may cause SPTB mRNA instability, resulting in insufficient spectrin protein synthesis and affecting the integrity and flexibility of the red blood cell membrane skeleton. This case report found that SPTB gene mutations may cause liver dysfunction and cirrhosis in addition to hereditary spherocytosis, and this finding expands the phenotypic spectrum of SPTB. This study confirmed that NGS can be used to diagnose hereditary spherocytosis. Identifying mutated genes can not only accurately treat diseases, but also avoid potential genetic risks and improve prenatal and postnatal care.

Cardiotoxicity of sanguinarine via regulating apoptosis and MAPK pathways in zebrafish and HL1 cardiomyocytes.

Sanguinarine, a plant phytoalexin, possesses extensive biological activities including antimicrobial, insecticidal, antitumor, anti-inflammatory and anti-angiogenesis effect. But its cardiotoxicity has rarely been studied. Here, we assess the cardiotoxicity of sanguinarine in vivo using larval zebrafish from 48 hpf to 96 hpf. The results show that sanguinarine caused severe malformation and the dysfunction of the heart including reductions of heart rate, red blood cell number, blood flow dynamics, stroke volume and increase of SV-BA distance, subintestinal venous congestion. Further studies showed that apoptosis in the zebrafish heart region was observed after sanguinarine exposure using TUNEL assay and AO staining method. In addition, the genes, such as sox9b, myl7, nkx2.5 and bmp10, which play crucial parts in the development and the function of the heart, were changed after sanguinarine treatment. caspase3, caspase9, bax and bcl2, apoptosis-related genes, were also altered by sanguinarine. Further studies were performed to study the cardiotoxicity in vitro using cardiomyocytes HL1 cell line. The results showed that remarkable increase of apoptosis and ROS level in HL1 cells were induced by sanguinarine. Moreover, the MAPK pathway (JNK and P38) were notably enhanced and involved in the cardiotoxicity induced by sanguinarine. Our findings will provide better understanding of sanguinarine in the toxic effect on heart.

circHUWE1 Exerts an Oncogenic Role in Inducing DDP-Resistant NSCLC Progression Depending on the Regulation of miR-34a-5p/TNFAIP8.

BACKGROUND: Circular RNAs (circRNAs) are reported as competing endogenous RNAs (ceRNAs) and play key roles in non-small-cell lung cancer (NSCLC) progression. Thus, this study was aimed at clarifying underlying molecular mechanisms of circHUWE1 in NSCLC. METHODS: The quantitative real-time polymerase chain reaction (RT-qPCR) and western blot analyses were used for examining circHUWE1, microRNA-34a-5p (miR-34a-5p), and tumor necrosis factor alpha-induced protein 8 (TNFAIP8). IC50 of cisplatin (DDP) in A549/DDP and H1299/DDP cells and cell viability were analyzed by the Cell Counting Kit 8 (CCK-8) assay. Colony forming assay was performed to assess colony forming ability. Cell apoptosis and cell cycle distribution were determined by flow cytometry. Migrated and invaded cell numbers were examined by transwell assay. The association among circHUWE1, miR-34a-5p, and TNFAIP8 was analyzed by dual-luciferase reporter and RNA immunoprecipitation assays. A xenograft experiment was applied to clarify the functional role of circHUWE1 in vivo. RESULTS: circHUWE1 was upregulated in NSCLC tissues and cells, especially in DDP-resistant groups. circHUWE1 downregulation inhibited DDP resistance, proliferation, migration, and invasion while it induced apoptosis and cell cycle arrest of DDP-resistant NSCLC cells, which was overturned by silencing of miR-34a-5p. TNFAIP8 was a functional gene of miR-34a-5p, and the suppressive effects of miR-34a-5p overexpression on DDP-resistant NSCLC progression were dependent on the suppression of TNFAIP8. circHUWE1 inhibition also delayed tumor growth of DDP-resistant NSCLC cells. CONCLUSION: circHUWE1 functioned as a promoter in DDP-resistant NSCLC by interaction with miR-34a-5p-TNFAIP8 networks, providing novel insight into DDP-resistant NSCLC diagnosis and treatment.

Primary central nervous system lymphoblastic B cell lymphoma located at cerebellum in a child: A case report and literature review.

INTRODUCTION: Primary central nervous system lymphoma (PCNSL) is extremely rare in pediatric population. We reported a case of PCNSL in a 3-year-old girl and reviewed the literature in the past three decades. CASE PRESENTATION: A 3-year-old girl presented with gait disturbance. A contrast-enhanced magnetic resonance image of the brain showed a solitary bulky mass in the left cerebellar hemisphere, hydrocephalus and cerebellar tonsillar hernia. Surgical resection was performed and the patient was diagnosed with primary central nervous system lymphoblastic B cell lymphoma. Then the patient received regular chemotherapy, including 6 cycles of chemotherapy containing high-dose methotrexate (HD-MTX). The patient remains alive 15 months after the diagnosis with no evidence of active disease, but suffered twice chronic subdural hematoma, which was treated by burr hole drainage. CONCLUSION: Lymphoblastic B cell lymphoma is a rare histologic subtype of pediatric PCNSL. Chemotherapy containing HD-MTX remains the most effective treatment. The patient should avoid head impact after surgical resection of the tumor to prevent chronic subdural hematoma.

Statistical Analysis on Rate Parameters of the H2-O2 Reaction System.

Quantitative rate determination of elementary reactions is a major task in the study of chemical kinetics. To ensure the fidelity of their determination, progressively tightened constraints need to be placed on their measurement, especially with the development of various notable experimental techniques. However, the evaluation of reaction rates and their uncertainties is frequently conducted with substantial subjectivity due to data source, thermodynamic conditions, sampling range, and sparsity. To reduce the extent of biased rate evaluation, we propose herein an approach of uncertainty-weighted statistical analysis, utilizing weighted average, and weighted least-square regression in statistical inference. Based on the backbone H2/O2 chemistry, rate data for each elementary reaction are collected from the time-history profile in shock tube experiments and high-level theoretical calculations, with their assigned weight inversely depending on uncertainty, which would overall avoid subjective assessments and provide more accurate rate evaluation. Aided by sensitivity analysis, the rates of a few key reactions are further constrained in the less investigated low- to intermediate-temperature conditions using high-fidelity flow reactor data. Good performance of the constructed mechanism is confirmed with validation against the target of the high-fidelity flow reactor data. This study demonstrates a systematic approach for reaction rate evaluation and uncertainty quantification.

Stable Organic Passivated Carbon Nanotube-Silicon Solar Cells with an Efficiency of 22.

The organic passivated carbon nanotube (CNT)/silicon (Si) solar cell is a new type of low-cost, high-efficiency solar cell, with challenges concerning the stability of the organic layer used for passivation. In this work, the stability of the organic layer is studied with respect to the internal and external (humidity) water content and additionally long-term stability for low moisture environments. It is found that the organic passivated CNT/Si complex interface is not stable, despite both the organic passivation layer and CNTs being stable on their own and is due to the CNTs providing an additional path for water molecules to the interface. With the use of a simple encapsulation, a record power conversion efficiency of 22% is achieved and a stable photovoltaic performance is demonstrated. This work provides a new direction for the development of high-performance/low-cost photovoltaics in the future and will stimulate the use of nanotubes materials for solar cells applications.

Role-playing: an Effective Method for Clinical Novitiate Teaching of Infectious Diseases.

OBJECTIVE: This study aims to apply the role-play method of teaching to clinical novitiate teaching of infectious diseases and assess the student feedback and learning effect. METHODS: The students were randomly divided into a role-playing group (taught using a role-playing method) and a standard group (taught using traditional method). Typical cases of hemorrhagic fever with renal syndrome (HFRS) with fever, hypertensive shock, and oliguria phase overlap as clinical manifestations were selected. Students in the role-playing group underwent pre-class preparation according to a well-designed script and performed the patient's consultation process of suspected HFRS in the classroom, followed by a discussion and questionnaire survey. The standard group underwent routine theory teaching. Teaching efficacy was evaluated by theoretical examination. RESULTS: The test scores and case analysis ability were higher for students in the role-playing group than in the standard group (p < 0.05). Nearly 90% of the students in the role-playing group gave positive feedback on the role-playing pedagogy and were willing to participate in its classroom implementation. CONCLUSION: Role-playing has positive effects on knowledge acquisition, skills upgrading, and attitudes related to medical teaching. Therefore, this method can be introduced in the teaching of other medical courses. SUPPLEMENTARY INFORMATION: The online version of this article (10.1007/s40670-020-01031-x) contains supplementary material, which is available to authorized users.

Developmental toxicity caused by sanguinarine in zebrafish embryos via regulating oxidative stress, apoptosis and wnt pathways.

Sanguinarine, derived from the root of Sanguinaria canadensis, have multiple biological activities, such as antimicrobial, insecticidal, antitumor, anti-inflammatory and anti-angiogenesis effect, but little is known about its toxicity on normal embryonic development. Here, we study the developmental toxicity using zebrafish model. Notably, sanguinarine caused a significant increase of the malformation rate and decrease of hatching rates and body length of zebrafish embryos. Sanguinarine also impaired the normal development of heart, liver and nerve system of zebrafish embryos. Further, the ROS level and MDA concentrations were remarkably increased, while the activity of T-SOD was decreased. In addition, obvious increase of apoptosis were observed by AO staining or TUNEL assay. Further studies showed that the oxidative stress-, apoptosis-related genes were changed, while genes of nrf2 and wnt pathways were inhibited by sangunarine. To sum up, our study will be helpful to understand the adverse effect of sanguinarine on embryonic development and the underlying molecular mechanism.