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Lower-extremity peripheral arterial disease (PAD) results in limb ischemia and is strongly associated with sarcopenia. This study aimed to retrospectively evaluate the association between the quantity of muscle mass in the lower extremities and the severity of vascular stenosis in PAD patients.Between January 2018 and August 2021, 128 patients with PAD and 53 individuals without PAD, diagnosed by computed tomography, were enrolled. The severity of stenosis of lower-extremity arteries was measured using a grading system. The muscle and fat mass areas were calculated in the abdomen at the L3 or L4 level, mid-thigh, and lower leg. Multivariable logistic regression was conducted to clarify the risk associated with low muscle mass. The difference in muscle mass between PAD and non-PAD patients was evaluated by using propensity score matching.A strong positive correlation between the abdomen muscle area and leg muscle area was observed. The muscle area and muscle index of the leg were lower in PAD patients. These changes occurred earlier than in the abdomen muscle area. The group with more severe artery stenosis had more muscle wasting in the lower extremities. Greater age, female, lower BMI, and PAD were associated with low muscle mass. After propensity score matching, the leg muscle area was still lower in PAD patients.There is a direct association between PAD and regional muscle wasting. This occurs earlier regionally in the lower extremities than in central muscles. Early diagnosis of PAD might prevent progressive muscle loss, improving disease outcome and quality of life.• Peripheral arterial disease is strongly associated with sarcopenia. • Muscle wasting in the lower extremities is earlier and more prominent than that in the abdomen. • More severe arterial stenoses are associated with higher muscle wasting in the lower extremities.

ObjectiveThe objective of this study was to identify prognostic factors in Hypertrophic cardiomyopathy patients with HFpEF, with a particular focus on the role of FT3 levels.Research Design and MethodsWe conducted a retrospective cohort study of 992 patients with HFpEF who were admitted to our two medical centers between 2009 and 2019. We collected demographic and clinical data, including FT3 levels, and conducted univariate and multivariate Cox analyses, KM survival curve analysis, and RSC curve analysis to identify prognostic factors and evaluate the non-linear predictive value of FT3.ResultsWe found that age, atrial fibrillation, and NT-proBNP levels were all significant prognostic factors in patients with heart failure. Additionally, FT3 levels were a significant independent predictor of all-cause mortality and cardiac transplantation. Patients with lower FT3 levels had worse long-term prognoses, and the critical value of FT3 was 2.885.ConclusionsOur findings suggest that FT3 levels are an important prognostic factor in patients with heart failure and should be considered when evaluating patient outcomes. Clinicians should monitor FT3 levels and consider interventions to maintain or improve thyroid function in patients with heart failure.Article HighlightsFT3 levels are a significant independent predictor of all-cause mortality and cardiac transplantation in Hypertrophic cardiomyopathy patients with HFpEFPatients with hypertrophic cardiomyopathy combined with HFpEF have a poorer long-term prognosis with lower FT3 levels, with a critical FT3 value of 2.885Age, atrial fibrillation, and NT-proBNP levels were also significant prognostic factors in Hypertrophic cardiomyopathy patients with HFpEFClinicians should monitor FT3 levels and consider interventions to maintain or improve thyroid function in Hypertrophic cardiomyopathy patients with HFpEF.

PDF file, 75K, Overexpression of CTMP enhances PI3K-mediated Akt phosphorylation.

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PDF file, 187K, The N-terminal domain, 1-64 a.a., of CTMP is required, but not sufficient, to induce Akt phosphorylation, colony formation and cell proliferation.

PDF file, 63K, Association of CTMP expression with prognosis of patients with different cancer type in 4 cohorts from Prognoscan database.

PDF file - 287K, Cisplatin-induced enrichment of CD133+ cells

PDF file - 289K, Carboplatin induced DNA damage and CD133+ cell enrichment

PDF file - 342K, Inhibition of cisplatin-induced enrichment of CD133+ cells by Notch1 knockdown

PDF file, 70K, PI3K inibitor blocked serum-induced Akt phosphorylation.

PDF file - 255K, The role of ABC transporters in cisplatin-induced multi-drug resistance to paclitaxol in H460 and H661 cell lines

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PDF file - 2.1MB, Cell differentiation and migration of GFP+ cells isolated from H460 cell line

PDF file, 114K, CTMP mRNA expression data adapted from GEO public available microarray database, GSE3744.

PDF file - 138K, The role of Notch signaling in enrichment of CD133+ cells and multi-drug resistance of H661 cells

The extraction conditions of polysaccharides from Portulaca oleracea L.（POP） were optimized and its effects on the colonic mucosa of mice with ulcerative colitis were studied. In this study, POP were extracted by ultrasonic and microwave synergism. The extraction process of POP was optimized by a single factor experiment and orthogonal design. HE staining was used to evaluate the pathological changes of colon tissues in mice. The results showed that the optimal extraction conditions were as follows: extraction time was 550 s, microwave power was 40 W, solid-liquid ratio (W/V) was 1:35, and extraction times were 3. Under these conditions, the extraction rate of POP was 3.80%. POP could improve the disease state of UC mice, and the high dose group could significantly reduce the DAI index. The results of the HE experiment showed that POP could reduce inflammatory infiltration and tissue damage of the colon in UC mice. This study provided a theoretical basis for the preparation of POP and its clinical application in the treatment of ulcerative colitis.

Context Limited studies have focused on the impact of subclinical hyperthyroidism (SHyper) on poor prognosis in patients with known coronary artery disease (CAD). Objective We implemented the present study to explore the association between SHyper and adverse cardiovascular events in CAD patients who underwent drug-eluting stent implantation. Methods We consecutively recruited 8283 CAD patients undergoing percutaneous coronary intervention (PCI). All subjects were divided into 2 groups according to their thyroid function: group 1 (euthyroidism group, n = 7942) and group 2 (SHyper group, n = 341). After 1:4 propensity score (PS) matching, 1603 patients (332 SHyper group and 1271 euthyroidism group) were selected. The primary endpoint was major adverse cardiovascular events (MACEs), a composite of cardiac mortality, nonfatal myocardial infarction (MI), and target vessel revascularization (TVR). Results Kaplan–Meier (K-M) survival analyses suggested that there was no significant difference in the primary endpoint and secondary endpoints (MACE: 11.4% vs 8.8%, log-rank P = .124; cardiac death: 1.2% vs 0.9%, log-rank P = .540; nonfatal MI: 5.7% vs 4%, log-rank P = .177; and TVR: 6% vs 4.7%, log-rank P = .303) in the PS-matched population. Cox regression analysis indicated that SHyper was not an independent risk factor for MACEs (HR 1.33, 95% CI 0.92-1.92, P = .127). Conclusion SHyper is not independently associated with adverse cardiovascular events in CAD patients undergoing PCI. More studies should be implemented in the future to assess the long-term predictive value of SHyper with thyrotropin levels

Limited studies have focused on the impact of high-sensitivity C-reactive protein (hsCRP) to albumin ratio (CAR) on cardiovascular outcomes in patients undergoing percutaneous coronary intervention (PCI). Hence, the present study evaluates the association between CAR and cardiovascular outcomes in patients undergoing drug-eluting stent (DES) implantation. We consecutively enrolled 9375 CHD patients undergoing DES implantation. All patients were divided into 3 groups according to their CAR: tertile 1 (CAR ≤.02, n=3125), tertile 2 (.02.06, n = 3125). The primary endpoint was major adverse cardiovascular and cerebrovascular events (MACCE). Kaplan-Meier analysis indicated that the incidences of MACCE and MI increased with high tertiles of the CAR (MACCE: 8.7 vs 10.5 vs 12.3%, log-rank P < .001; MI: 3.3 vs 4.0 vs 4.7%, long-rank P = .015). Cox regression analysis suggested that CAR was an independent risk factors for MACCE (HR per standard deviation (SD) increase: 1.07, 95% CI, 1.01–1.14, P = .024), and MI (HR per SD increase: 1.11, 95% CI, 1.01–1.22, P = .028). In conclusion, the CAR is an independent predictor of MACCE and MI in CHD patients.

Hydroarylation of alkynes with unactivated C(sp2)−H bonds via chelated C−H metalation mainly occurs at γ-position to the coordinating atom of directing groups via stable 5-membered metallacycles, while β-C(sp2)−H bond-involved hydroarylation has been a formidable challenge. Herein, we used a phosphine oxide-ligated Ni−Al bimetallic catalyst to enable β-C−H bond-involved hydroarylations of alkynes via a rare 7-membered nickelacycle.

Background It is unclear whether bisphosphonates are associated with risk of cancers. Therefore, this meta-analysis aimed to evaluate the effect of bisphosphonates on overall cancers. Methods A search in Pubmed, Embase, Cochrane Library and Web of Science databases was conducted, from the inception date of each resource to September 26, 2019. The summarised effect estimates with 95% CIs were calculated using a random-effect model. Heterogeneity and publication bias were explored. Results Thirty-four articles were included in this study (4,508,261 participants; 403,196 cases). The results revealed that bisphosphonates significantly decreased the risk of colorectal cancer (RR = 0.89, 95% CI: 0.81–0.98), breast cancer (RR = 0.87, 95% CI: 0.82–0.93) and endometrial cancer (RR = 0.75, 95% CI: 0.61–0.94), but no significant association was observed in all-cause cancer. Furthermore, nitrogen-containing bisphosphonates only had protective effects both on breast cancer (RR = 0.94, 95% CI: 0.90–0.99) and endometrial cancer (RR = 0.70, 95% CI: 0.54–0.92). Non-nitrogen-containing bisphosphonates tended to increase the risk of liver cancer (RR = 2.14, 95% CI: 1.23–3.72) and pancreas cancer (RR = 1.75, 95% CI: 1.32–2.33). Conclusion Bisphosphonates are significantly associated with risk reduction of colorectal, breast and endometrial cancer, especially nitrogen-containing bisphosphonates. It should be noted that non-nitrogen-containing bisphosphonates might increase the risk of liver and pancreas cancer. Large prospective cohort studies are needed to find the causal association between bisphosphonates and risk of cancers.

Cancer cells with mesenchymal attributes potentially display chemoresistance. Cancer stem cells (CSCs), which are intrinsically resistant to most chemotherapy agents, exhibit considerable phenotypic heterogeneity in their epithelial versus mesenchymal states. However, the drug response of CSCs in the epithelial and mesenchymal states has not been completely investigated. In this study, we found that epithelial-type (E-cadherinhigh/CD133high) CSCs displayed a higher sphere formation ability and chemoresistance than mesenchymal-type (E-cadherinlowCD133high) CSCs. Gene expression profiling of the CSC and non-CSC subpopulations with distinct epithelial-to-mesenchymal transition (EMT) states showed that MyoD family inhibitor domain-containing (MDFIC) was selectively upregulated in epithelial-type CSCs. Knockdown of MDFIC sensitized epithelial-type CSCs to chemotherapy agents. Ectopic expression of MDFIC increased the chemoresistance of mesenchymal-type CSCs. In a tissue microarray, high MDFIC expression was associated with poor prognosis of non-small cell lung cancer (NSCLC) patients. A mechanistic study showed that the MDFIC p32 isoform, which is located in the cytoplasm, interacted with the destruction complex, Axin/GSK-3/β-catenin. This interaction stabilized β-catenin by inhibiting β-catenin phosphorylation at S33/37 and increased the nuclear translocation and transcriptional activity of β-catenin. Knockdown of β-catenin decreased MDFIC-enhanced chemoresistance. These results suggested that the upregulation of MDFIC enhanced the chemoresistance of epithelial-type CSCs by elevating β-catenin activity. Thus, targeting MDFIC-regulated β-catenin signaling of epithelial-type CSCs may be a potential strategy to overcome chemoresistance in NSCLC.

Simple Summary Conventional serum markers such as carcinoembryonic antigen (CEA), squamous cell carcinoma antigen (SCC), and tissue polypeptide antigen (TPA) have a low sensitivity in predicting the prognosis of locoregional esophageal squamous cell carcinoma cell (ESCC). In our clinical study, we found high serum elafin to be an independent outcome predictor for stage I-IIIA ESCC, considering T, N, overall stage, and treatment. In vitro experiments showed that adding recombinant elafin drove ESCC cell proliferation, migration and invasion, while shRNA attenuated elafin levels, abrogating those effects. Our results suggested serum elafin might be a noninvasive biomarker to predict the outcome of locoregional ESCC and could potentially be used as a therapeutic target. Abstract Esophageal squamous cell carcinoma (ESCC) is a highly aggressive tumor known to have locally advanced and metastatic features which cause a dismal prognosis. We sought to determine whether elafin, a non-invasive and secretory small-molecule marker, could be used to predict prognosis in locoregional ESCC patients in human and in vitro studies. In our human study, 119 subjects were identified as having incident and pathologically-proved ESCC with stage I-IIIA tumors from southern Taiwan between 2000 and 2016. We measured their serum elafin levels at baseline and followed them until the date of cancer death or until January 2020, the end of this study. Those with high serum elafin levels were found to have a 1.99-fold risk (95% confidence interval: 1.17–3.38) shorter survival than those who did not. In our in vitro experiments, elevated elafin levels were found to drive ESCC cell proliferation, migration and invasion, while attenuation of elafin level by shRNA abrogated those effects. We concluded that elafin promotes ESCC motility and invasion and leads to a worse clinical prognosis in ESCC patients without distant metastasis.

Background and purpose Mitochondrial dysfunction plays a role in the progression of cardiovascular diseases including heart failure. 3-Hydroxy-3-methylglutaryl-CoA reductase inhibitors (statins), which inhibit ROS synthesis, show cardioprotective effects in chronic heart failure. However, the beneficial role of statins in mitochondrial protection in heart failure remains unclear. Experimental approach Rats were treated with angiotensin II (1.5 mg·kg-1 ·day-1 ) or co-administered simvastatin (oral, 10 mg·kg-1 ) for 14 days; and then administration was stopped for the following 14 days. Cardiac structure/function was examined by wheat germ agglutinin staining and echocardiography. Mitochondrial morphology and the numbers of lipid droplets, lysosomes, autophagosomes, and mitophagosomes were determined by transmission electron microscopy. Human cardiomyocytes were stimulated, and intracellular ROS and mitochondrial membrane potential (ΔΨm ) changes were measured by flow cytometry and JC-1 staining, respectively. Autophagy and mitophagy-related and mitochondria-regulated apoptotic proteins were identified by immunohistochemistry and western blotting. Key results Simvastatin significantly reduced ROS production and attenuated the disruption of ΔΨm . Simvastatin induced the accumulation of lipid droplets to provide energy for maintaining mitochondrial function, promoted autophagy and mitophagy, and inhibited mitochondria-mediated apoptosis. These findings suggest that mitochondrial protection mediated by simvastatin plays a therapeutic role in heart failure prevention by modulating antioxidant status and promoting energy supplies for autophagy and mitophagy to inhibit mitochondrial damage and cardiomyocyte apoptosis. Conclusion and implications Mitochondria play a key role in mediating heart failure progression. Simvastatin attenuated heart failure, induced by angiotensin II, via mitochondrial protection and might provide a new therapy to prevent heart failure.

Fluorescent probes have become an indispensable tool in the detection and imaging of biological and disease-related analytes due to their sensitivity and technical simplicity. In particular, fluorescent probes with far-red to near-infrared (FR-NIR) emissions are very attractive for biomedical applications. However, many available FR-NIR fluorophores suffer from small Stokes shifts and sometimes low quantum yields, resulting in self-quenching and low contrast. In this work, we describe the rational design and engineering of FR-NIR 2,4,6-triphenylpyrylium-based fluorophores (TPP-Fluors) with the help of theoretical calculations. Our strategy is based on the appending of electron-donating substituents and fusing groups onto 2,4,6-triphenylpyrylium. In contrast to the parent TPP with short emission wavelength, weak quantum yields, and low chemical stability, the obtained novel TPP-Fluors display some favorable properties, such as long-wavelength emission, large Stokes shifts, moderate to high quantum yields, and chemical stability. TPP-Fluors demonstrate their biological value as mitochondria-specific labeling reagents due to their inherently positive nature. In addition, TPP-Fluors can also be applied to develop ratiometric fluorescent probes, as the electron-donating ability of the 2,6-phenyl substituents is closely correlated with their emission wavelength. A proof-of-concept ratiometric probe has been developed by derivatizing the amino groups of TPP-Fluor for the detection and imaging of nitroreductase in vitro and in hypoxic cells.

We investigated the storage lower urinary tract symptoms (LUTS) before and after the first dose of coronavirus disease 2019 (COVID-19) vaccine and the association between pre-vaccinated overactive bladder (OAB) and the worsening of storage LUTS following COVID-19 vaccination. This cross-sectional study in a third-level hospital in Taiwan used the validated pre- and post-vaccinated Overactive Bladder Symptom Score (OABSS). Diagnosis of OAB was made using pre-vaccinated OABSS. The deterioration of storage LUTS was assessed as the increased score of OABSS following vaccination. Of 889 subjects, up to 13.4% experienced worsened storage LUTS after vaccination. OAB was significantly associated with an increased risk of worsening urinary urgency (p = 0.030), frequency (p = 0.027), and seeking medical assistance due to urinary adverse events (p < 0.001) after vaccination. The OAB group faced significantly greater changes in OABSS-urgency (p = 0.003), OABSS-frequency (p = 0.025), and total OABSS (p = 0.014) after vaccination compared to those observed in the non-OAB group. Multivariate regression revealed that pre-vaccinated OAB (p = 0.003) was a risk for the deterioration of storage LUTS. In conclusion, storage LUTS may deteriorate after vaccination. OAB was significantly associated with higher risk and greater changes in worsening storage LUTS. Storage LUTS should be closely monitored after COVID-19 vaccination, especially in those OAB patients.

Epidermal growth factor tyrosine kinase inhibitors (EGFR-TKIs) are currently the most effective treatment for non-small cell lung cancer (NSCLC) patients, who carry primary EGFR mutations. However, the patients eventually develop drug resistance to EGFR-TKIs after approximately one year. In addition to the acquisition of the EGFR T790M mutation, the activation of alternative receptor-mediated signaling pathways is a common mechanism for conferring the insensitivity of EGFR-TKI in NSCLC. Upregulation of the Mer receptor tyrosine kinase (MERTK), which is a member of the Tyro3-Axl-MERTK (TAM) family, is associated with a poor prognosis of many cancers. The binding of specific ligands, such as Gas6 and PROS1, to MERTK activates phosphoinositide 3-kinase (PI3K)/Akt and mitogen-activated protein kinase (MAPK) cascades, which are the signaling pathways shared by EGFR. Therefore, the inhibition of MERTK can be considered a new therapeutic strategy for overcoming the resistance of NSCLC to EGFR-targeted agents. Although several small molecules and monoclonal antibodies targeting the TAM family are being developed and have been described to enhance the chemosensitivity and converse the resistance of EGFR-TKI, few have specifically been developed as MERTK inhibitors. The further development and investigation of biomarkers which can accurately predict MERTK activity and the response to MERTK inhibitors and MERTK-specific drugs are vitally important for obtaining appropriate patient stratification and increased benefits in clinical applications.

Purpose. The present study investigated the risk factors for high myopia in adulthood, with a focus on the age at which children wore their first spectacles. Methods. Adults aged between 20 and 45 years were invited to complete a questionnaire about age, sex, current refractive error, high myopia in parents, early onset of myopia presented by the age of the first myopic spectacle prescription, refractive power of the first spectacles, and life habits at different educational stages. The associations between these factors and high myopia in adulthood were then evaluated and analyzed. Results. In total, 331 participants were enrolled. Their average refractive error was −4.03 diopters, and high myopia was noted in 27.5% of the study participants. Only 3.3% of participants had fathers with high myopia, while 6.0% had mothers with high myopia. The participants received their first myopic spectacle prescription at a mean age of 13.35 years, with a mean refractive error of −1.63 diopters. The significant risk factors for developing high myopia in adult life were earlier age of the first spectacles prescribed ( p < 0.001 ), higher refractive power of the first spectacles ( p < 0.001 ), mother with high myopia ( p = 0.015 ), and after-school class attendance in senior high school ( p = 0.018 ). Those who wore their first spectacles at

Background: To investigate the risk factors for high myopia in adulthood, especially as it relates to the age of first spectacle wearing.Methods: A retrospective study enrolled adults aged between 20 and 45 years being invited to complete a questionnaire about age, sex, current refractive error, high myopia in parents, age at first spectacle use, refractive power of the first spectacles, and life habits at different educational stages. The association between these factors and high myopia were then evaluated and analyzed.Results: In total, 331 participants were enrolled. Their average refractive error was -4.03 diopters, and high myopia was noted in 27.5% of the study population. Only 3.3% of participants had fathers with high myopia, while 6.0% had mothers with high myopia. The participants received their first spectacles at a mean age of 13.35 years, with a mean refractive error of -1.63 diopters.The significant risk factors for developing high myopia in adult life were earlier age at first spectacle use (p < 0.001), higher refractive power of first spectacles (p < 0.001), mother with high myopia (p = 0.015), and after-school class attendance in senior high school (p = 0.018). Those who wore their first spectacles at < 9 years of age were more predisposed to high myopia than those who did so at ≧ 13 years, with an odds ratio of 24.891, while the odds ratio for those aged between 10 and 12 years was 5.294.Conclusions: The present study shows that earlier age at first spectacle use, higher myopic refraction of first spectacles, mothers with high myopia, and after-school class attendance in senior high school are predictive factors for high myopia in adulthood. The most important predictive factor is earlier age at first spectacle use, which emphasizes earlier myopia control is a protective factor for high myopia in adulthood.

Hereby, the case of an 8-month-old girl diagnosed with partial anomalous left pulmonary artery (PLPA) is presented. Echocardiography and computed tomography (CT) examination demonstrated that the anomalous artery originated from the right pulmonary artery supplying the left upper lobe. PLPA is sometimes associated with tracheobronchial anomaly and congenital cardiovascular defects. A relationship between PLPA and Kabuki syndrome has also been suggested. Echocardiography and CT angiography can be used as accurate tools for identifying an anomalous left pulmonary artery and adjacent abnormal anatomic structures.

Ethnopharmacological relevance Gynura divaricata subsp. formosana is a widely used traditional herbal medicine for treating liver disorders such as hepatitis and liver cancer in Taiwan. Aim of the study This study was aimed to evaluate the anti-cancer and cancer stabilization effect of water extract of the aerial part of G. divaricata (GD extract) both in vitro and in vivo. Materials and methods Cytotoxicity and anti-proliferative effects of GD extract alone and in combination with cisplatin were determined by alamarBlue and clonogenic assay. Cancer stem cell (CSC) inhibition and the expression of CSC markers were revealed by sphere formation assay and real-time PCR (qPCR). The in vivo anti-cancer effect of GD extract was evaluated in Huh7 xenograft mice model and Ki-67 expression were also measured. The activity of Wnt signalling and the expression level of Wnt target genes and β-catenin were determined by luciferase reporter assay, qPCR, immunoblotting and IHC. Results Moderate cytotoxicity of GD extract in liver cancer cells was observed. GD extract sensitized Huh7 cells to cisplatin treatment. Interestingly, GD extract inhibited cancer sphere formation and reduced the expression of CSC markers. Importantly, GD extract suppressed Huh7 tumor growth, Ki-67 expression and prolonged the anti-liver cancer effect of cisplatin in vivo. Treatment of GD extract resulted in reductions of Wnt reporter activity and the expression of Wnt target genes. Moreover, suppression of β-catenin were observed in both GD extract treated Huh7 spheres and xenograft tumors. Conclusion Accordingly, our findings suggest that G. divaricata may target liver CSC by suppressing the Wnt pathway and the combination of G. divaricata and cisplatin could be a candidate regimen for treating HCC.

Histone deacetylase 6 (HDAC6), a member of the HDAC enzymes, has been reported to play substantial roles in many cellular processes. Evidence shows that deregulation of HDAC6 may be involved in the progression of some cancers, neurodegenerative diseases, and inflammatory disorders. However, little is known regarding the effect of post-translational modification of HDAC6 on cellular localization and biological functions. In the present study, we identified four phosphorylation sites on HDAC6 under normal conditions by mass spectrometry analysis. Two phosphorylation sites, pSer22 and pSer412, are recognized as Pin1 (peptidyl-prolyl cis/trans isomerase NIMA-interacting 1) substrates. Pin1 can interact with HDAC6 and be involved in HDAC6-mediated cell motility. Pin1 depletion abrogates HDAC6-induced cell migration and invasion in H1299 lung cancer cells. The findings of this study suggest that Pin1 might regulate HDAC6-mediated cell motility through alteration of protein conformation and function. Our results indicate the complexity of activity regulation between HDAC6 and Pin1, expanding knowledge regarding the multifunctional roles of Pin1 in tumorigenesis and cancer progression.

IntroductionThe thyroid cancer incidence has been increasing all over the world. However, the aetiology of thyroid cancer remains unclear. A growing body of evidence suggested exposure to persistent organic pollutants (POPs) may play a role in the initiation of thyroid cancer, but the results are generally inconsistent across studies. This review aims to synthesise the evidence for the health effects of POPs on the risk of thyroid cancer.Methods and analysisThis protocol was reported in accordance to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses Protocols (PRISMA) statements. A comprehensive search, including electronic database search (eg, PubMed, Embase, ProQuest and CNKI), website search and manual search, will be performed to identify all eligible studies. The Population, Exposure, Comparator and Outcome framework was used to clarify the inclusion and exclusion criteria. The Newcastle-Ottawa Scale will be used to assess the quality of included studies. Maximally adjusted effect estimates from individual studies will be summarised with random-effect models in a conservative manner. I2 statistics and Q-tests will be used to test the heterogeneity across studies. We will perform extensive sensitivity analyses, such as confounding risk ratio (confounding), E-value, fixed-effect models, excluding the most relatively weighted study, including only the high-quality studies and many predesigned subgroup analyses, etc. The findings will be reported in accordance to the PRISMA guidelines.Ethics and disseminationEthical approval is not required in this systematic review of published literatures. The results will be published in a peer-reviewed journal and presented at relevant conferences.PROSPERO registration numberCRD42020181343.

Prenatal congenital lobar fluid overload (CLFO), which was first described by Ramsay and Byron, is identical to postnatal congenital lobar overinflation. It is characterized by progressive lobar overexpansion that compresses the other adjacent lung lobes. The underlying cause can be an intrinsic cartilaginous abnormality or an extrinsic airway compression. It may be associated with cardiovascular anomalies in 12%-14% of cases and affects males more frequently than females. Most cases are diagnosed postnatally, but early antenatal diagnosis and sequential follow-up are attempted for early treatment, if clinically indicated. This article provided a thorough review of CLFO, including prenatal diagnosis and differential diagnoses, as well as comprehensive illustrations of the perinatal imaging findings of CLFO. Prenatal diagnosis of fetal lung lesions should include CLFO in the differential diagnosis and prompt investigation for associated anomalies.

We report here a single-benzene based fluorescent framework, amino-terephthalonitrile, denoted SB-Fluor. This scaffold displays versatile emission wavelength tunability via structure modification, covering the full visible light spectrum, both in the solution and solid state. Moreover, one molecule, SBF3, exhibits polymorphism-dependent reversible mechanochromic luminescence.

The novel ratiometric fluorescent probe HPQRB with an ESIPT effect based on Michael addition for highly sensitive and fast detection of sulfite in living HepG2 cells is reported. HPQRB can be easily synthesized by a two‐step condensation reaction. HPQRB has a large emission shift (Δλ=116 nm), which is beneficial for fluorescence imaging research, and its sulfite‐responsive site is based on a rhodamine‐like structure with the emission peak at 566 nm, which decreases with increasing sulfite concentration. and its HPQ structure always has an ESIPT effect throughout the reaction process, keeping the emission peak at 450 nm as a self‐reference. In particular, HPQRB has high selectivity for sulfite and responds quickly (within 30 s) with a low detection limit (44 nM). Furthermore, HPQRB has been successfully used for fluorescence imaging of sulfite in HepG2 cells, demonstrating the superior ability to detect sulfite under physiological conditions.

Deposition of atoms or molecules on a solid surface is a flexible way to prepare various novel two-dimensional materials if the growth conditions, such as suitable surface and optimum temperature, could be predicted theoretically. However, prediction challenges modern theory of material design because the free energy criteria can hardly be applied to this issue due to the long-standing problem in statistical physics of the calculations of the free energy. Herein, we present an approach to the problem by the demonstrations of graphene and &gamma, graphyne on the surface of copper crystal, as well as silicene on a silver substrate. Compared with previous state-of-the-art algorithms for calculations of the free energy, our approach is capable of achieving computational precisions at least 10-times higher, which was confirmed by molecular dynamics simulations, and working at least four orders of magnitude faster, which enables us to obtain free energy based on ab initio calculations of the interaction potential instead of the empirical one. The approach was applied to predict the optimum conditions for silicene growth on different surfaces of solid silver based on density functional theory, and the results are in good agreement with previous experimental observations.

During the past decade, sustainability science has rapidly developed into a globally well-recognized and important new science of the 21st century. However, sustainability science has not received much attention from scientists and practitioners in China where sustainable development and ecological civilization have been prominent themes. To promote the development of sustainability science in China, Wu, et al. (2014) published the first in-depth review on the subject in Chinese, entitled What is sustainability science? Here, we revisit the question, and discuss the relationship between sustainability science and sustainable development research, the scientific paradigm and the core research questions of sustainability science. Our review of the recent advances in this field reveals contrasting trends for the world versus China. On the one hand, the world is witnessing sustainability science maturing with global momentum to systematically advance sustainability research and education. On the other hand, China greatly lags behind developed countries and South Africa, albeit the great deal of new passion and desire for sustainable development. To promote the science and practice of sustainability in China, we propose a trinity strategy: 1) bringing in from the global community to guide Chinese practices in sustainable development; 2) reaching out to the global community to share Chinese wisdom of sustainable development; and 3) integrating traditional Chinese philosophy with western science to lead the development of sustainability science.近10年来,可持续性科学蓬勃发展,已成为21世纪全球普遍关注的一个重要的新科学领域.然而,在大力提倡可持续发展和生态文明建设的中国,可持续性科学尚未引起科学家和实践者的足够重视.为促进可持续性科学在中国的发展,2014年邬建国等曾撰文介绍什么是可持续性科学.本文进一步探讨了这一问题,并补充阐述了可持续性科学与可持续发展研究的关系、可持续性科学的科学范式及其8个基本论题.基于对可持续性科学发展动态的分析,作者认为,一方面,可持续性科学已进入系统推进的成熟发展期;另一方面,虽然我国可持续发展研究、实践与教育的热情高涨,但在可持续性科学领域起步较晚,落后于主要发达国家和南非.为此,本文在文献综述的基础上,提出促进中国发展可持续性科学的ldquo;三位一体rdquo;策略:一是ldquo;请进来rdquo;以服务中国实践;二是ldquo;走出去rdquo;以贡献中国智慧;三是ldquo;中西医结合rdquo;以引领学科发展.

Background: Esophageal squamous cell carcinoma (ESCC) is the major type of esophageal cancer in Asia and demonstrates poor survival rates following a therapeutic regimen. Methods: Cancer stem cells (CSCs) are responsible for tumor initiation, progression, and treatment failure in cancers. Therefore, identification and characterization of CSCs may help to improve clinical outcomes for ESCC patients. Tumor sphere formation assay are performed to isolate cancer stem-like ESCC cells. QRT-PCR, tumor initiation, metastasis, CCRT treatment are used to evaluate ESCC cells’ stemness properties in vitro and in vivo. Results: The authors’ data demonstrates that cancer stem-like ESCC cells harbored stemness characteristics including self-renewal, differentiation, and transdifferentiation, and possess tumor initiation, metastasis, and treatment inefficiency properties. For the identification of useful biomarkers of cancer stem-like ESCC cells, the authors further identified that CLDN4 was upregulated in cancer stem-like ESCC cells when compared with bulk cancer cells. High-CLDN4 cells harbored stemness and cisplatin/concurrent chemoradiation therapy (CCRT) resistance properties and a high level of CLDN4 was correlated with poor prognosis and poor CCRT response in ESCC patients. Importantly, thiamine tetrahydrofurfuryl disulfide (TTFD) decreased CLDN4 and attenuated stemness in ESCC cells, and TTFD combined with CCRT improved CCRT response in vivo. Conclusions: CLDN4 was suggested as prognostic and a CCRT response indicator for ESCC patients. TTFD combined with CCRT has potential to improve ESCC patient’s clinical outcomes in the future.

Coxsackievirus, a common pathogen causing pediatric infection, typically causes a mild, nonspecific illness with low-grade fever, but can cause severe illness on rare occasions. Encephalitis is an uncommon but important complication of coxsackievirus infection. The magnetic resonance imaging (MRI) findings of coxsackievirus B3 (CVB3) encephalitis have not been reported in the literature, and there are few descriptions of MRI findings of encephalitis induced by coxsackieviruses of other serotypes. We report the MRI findings of CVB3 encephalitis in a two-year-old girl, review the MRI findings in previously reported cases of pediatric coxsackievirus encephalitis, and present the MRI characteristics of coxsackievirus encephalitis.

Clinical usage of botulinum neurotoxin (BoNT) in ophthalmology has dramatically increased since the 1980s and has become one of the most widely used agents for treating facial movement disorders, autonomic dysfunction and aesthetic wrinkles. Despite its high efficacy, there are some complications with periocular BoNT injections due to its chemodenervation effect. Among these, there is still controversy over the BoNT effect on tear film homeostasis and the ocular surface. A periocular BoNT injection could dry the eye by reducing tear production of the lacrimal gland and increase tear evaporation due to potential eyelid malposition and abnormal blinks. On the contrary, the injection of BoNT in the medial eyelids could treat dry eye disease by impairing lacrimal drainage. Regarding the ocular surface change, corneal astigmatism and high-order aberrations may decrease due to less eyelid tension. In conclusion, the entire awareness of the effect of BoNT and the patients’ ocular condition is crucial for successful and safe results.

Non-small-cell lung cancer (NSCLC) is a deadly malignancy with a high prevalence worldwide. A reliable biomarker that can predict the prognosis is required to determine the therapeutic strategy. TIP30 was first identified as a tumor suppressor. A number of mechanistic studies indicated that the downregulation of TIP30 enhances the stemness, migration and survival of NSCLC cells. However, the clinical relevance of TIP30 for the prognosis of NSCLC is unknown. From a meta-analysis of public microarray datasets, we showed the upregulation of TIP30 mRNA expression was associated with worse overall survival of NSCLC patients, which contradicted the tumor suppressive role of TIP30. It is worth noting that the TIP30 mRNA expression was not correlated with its protein expression in 15 NSCLC cell lines. The results from the immunohistochemistry of a tissue microarray showed the downregulation of the TIP30 protein expression was associated with a higher risk of metastasis. In addition, the decrease in TIP30 protein was correlated with worse overall and progression-free survival of the NSCLC patients. Multivariate analysis suggested the loss of TIP30 protein was an independent factor to predict the poor prognosis of NSCLC. Our data indicated that TIP30 protein, not mRNA, would be a potential prognostic biomarker of NSCLC.

Ionic polyurethane (IPU) was synthesized as shape memory materials. Poly (tetramethylene ether) glycol with 2000g/mol number average molecular weight were used as soft segment, 4,4-methylenebis (phenyl isocyanate), and 1,2-dihydroxy-3-propanesulfonic acid salt were used to compose the segment of SMP materials. The structure and properties of these IPU films were characterized by Fourier Transform infrared, X-ray diffraction, Thermal gravimetric analysis and Differential scanning calorimeter. The results showed that the glass transition temperature of the IPU increased with the increase of hard segment content. The physical properties in terms of swelling property, water absorption and ion-exchange capacity increased with the improving of sulfonic group content in IPU. The shape memory property of IPU exhibited that the shape fixity ratio and recovery rate improved remarkably with the increase of hard segment content.