Simultaneously Improving the Optical, Dielectric, and Solubility Properties of Fluorene-Based Polyimide with Silyl Ether Side Groups.

Three fluorene-based polyimides with silyl ether groups (Si-PIs) were successfully synthesized by a simple and efficient silicon etherification reaction of hydroxyl-containing polyimides (OH-PIs) and tert-butylchlorodiphenylsilane (TBDPSCl), and their structures were confirmed by 1H NMR and IR spectra. The bulky nonpolar tert-butyldiphenylsilyl (TBDPS) side groups in the modified PI unit instead of the strong electron donor -OH group is conducive to decreasing electronic conjugation and charge transfer (CT) interaction along the PI chain. Accordingly, the optical, dielectric, and solubility properties of the modified Si-PI films are simultaneously improved compared with the precursor OH-PI films. The modified Si-PI films demonstrate a meaningful enhancement in the transmittances at a wavelength of 400 nm (T 400 ) to 74-81% from 42 to 55% of OH-PI films and the regeneration of fluorescence characteristics. The dielectric constant and loss of Si-PI films are also obviously reduced to 2.63-2.75 and 0.0024-0.0091 at 1 kHz from 4.19 to 4.78 and 0.0173-0.0295 of OH-PI films, respectively, due to substituted with the bulky nonpolar TBDPS groups to increase the free volume and hydrophobicity of Si-PI films. The solubility of Si-PIs in low- or nonpolar solvents (such as CHCl3, CH2Cl2, acetone, and toluene) is significantly improved. Furthermore, Si-PI films still maintain relatively good thermal properties with the 5% weight loss temperature (T 5% ) in the range 470-491 °C under a nitrogen atmosphere and the glass transition temperature (T g ) in the range 245-308 °C.

LBX2-AS1 as a Novel Diagnostic Biomarker and Therapeutic Target Facilitates Multiple Myeloma Progression by Enhancing mRNA Stability of LBX2.

Objective: Multiple myeloma (MM) represents a common age-associated malignancy globally. The function and underlying mechanism of antisense lncRNA LBX2-AS1 remain ambiguous in multiple myeloma (MM). Herein, we aimed to observe the biological implication of this lncRNA in MM. Methods: RT-qPCR was employed to examine circulating LBX2-AS1 and LBX2 in 60 paired MM and healthy subjects. Correlation between the two was analyzed by Pearson test. Under transfection with shLBX2-AS1, proliferation and apoptosis were evaluated in MM cells through CCK-8, colony formation and flow cytometry. LBX2 expression was examined in MM cells with shLBX2-AS1 or pcDNA3.1-LBX2 transfection. Following treatment with cycloheximide or actinomycin D, LBX2 expression was examined in pcDNA3.1-LBX2-transfected MM cells at different time points. Rescue assays were then presented. Finally, xenograft tumor models were established. Results: Circulating LBX2-AS1 was up-regulated in MM patients and positively correlated to LBX2 expression. Area under the curve (AUC) of LBX2-AS1 expression was 0.7525. Its up-regulation was also found in MM cells and primarily distributed in cytoplasm. LBX2-AS1 knockdown distinctly weakened proliferative ability and induced apoptosis in MM cells. Overexpressing LBX2-AS1 markedly strengthened LBX2 expression by increasing its mRNA stability. Rescue assays showed that silencing LBX2-AS1 distinctly weakened the pcDNA3.1-LBX2-induced increase in proliferation and decrease in apoptosis for MM cells. Silencing LBX2-AS1 markedly weakened tumor growth. Conclusion: Our data demonstrated that circulating LBX2-AS1 could be an underlying diagnostic marker in MM. Targeting LBX2-AS1 suppressed tumor progression by affecting mRNA stability of LBX2 in MM. Hence, LBX2-AS1 could be a novel therapeutic marker against MM.

Hollow Lindqvist-like-Shaped {V6} Cluster-Based Metal-Organic Framework for the Highly Efficient Detoxification of Mustard Gas Simulant.

A polyoxovanadate-based nickel-organic framework, [Ni(bib)2]{V2O6}({V6}-MOF, bib = 1,4-bis(1H-imidazoly-1-yl)benzene), was facilely prepared under gentle hydrothermal conditions and structurally characterized. Single-crystal X-ray diffraction analysis indicates that the {V6} cluster in the {V6}-MOF is constructed of two VO5 tetragonal pyramids and four VO4 tetrahedrons via the apex sharing of O atoms, presenting a hollow Linqvist-like structure, which is different from these reported hexanuclear vanadium clusters. The {V6}-MOF not only expands the structure of polyoxovanadates (POVs) but also catalyzes the rapid detoxification of mustard gas simulant (2-chloroethyl ethyl sulfide, CEES) at 25 °C. The catalytic results were determined by means of GC, GC-MS, and 1H NMR. Using {V6}-MOF as a heterogeneous catalyst, CEES underwent catalyzed oxidation to only nontoxic product 2-chloroethyl ethyl sulfoxide (CEESO) within 40 min, and the conversion and selectivity were almost 100%. In addition, {V6}-MOF exhibits high sustainability, and no obvious reductions in conversion and selectivity are observed after five runs.

Silencing of long non­coding RNA HRIM protects against myocardial ischemia/reperfusion injury via inhibition of NF­κB signaling.

Myocardial ischemia/reperfusion injury (MI/RI) following cardiac surgery is a leading cause of morbidity and mortality worldwide. The aim of the present study was to investigate the role of long non­coding RNA hypoxia/reoxygenation injury­related factor in myocytes (HRIM) on cardiac function following MI/RI. After establishing an MI/RI model, hemodynamic indices were detected via transthoracic echocardiography. The proliferative and apoptotic capacities of H9C2 cells subjected to oxygen­glucose deprivation/reoxygenation were detected via Cell Counting Kit­8 assay and flow cytometry, respectively. TNF­α, IL­1ß, IL­6, lactate dehydrogenase (LDH) and creatine kinase (CK) levels were measured via ELISA. The expression levels of NF­κB­associated proteins were detected via western blotting. The expression levels of HRIM were increased in the myocardial tissue of MI/RI rats and H9C2 cells. The infarct size was significantly increased following induction of MI/RI. Moreover, increased HRIM expression levels suppressed hemodynamics in MI/RI rats. Knockdown of HRIM increased cell proliferation and decreased apoptosis as well as the protein levels of phosphorylated (p)­NF­κB p65/NF­κB p65, p­IkBα/IkBα, TNF­α, IL­1ß, IL­6, LDH and CK in H9C2 cells; however, these effects were attenuated via activation of NF­κB signaling. Silencing of HRIM ameliorated MI/RI injury and alleviated inflammation via inactivating the NF­κB signaling pathway.

Antarctic Krill Oil Attenuates Oxidative Stress via the KEAP1-NRF2 Signaling in Patients with Coronary Heart Disease.

BACKGROUND: Antarctic krill oil (AKO) has strong antioxidant activities and is effective for alleviating coronary heart disease (CHD). Kelch-like ECH-associated protein 1-NF-E2-related factor 2 (KEAP1-NRF2) axis is a crucial antioxidant signaling pathway. Thus, AKO may exert its antioxidant effects on CHD patients via KEAP1-NRF2 signaling. METHODS: AKO fatty acid (FA) profiles were analyzed by using gas chromatography (GC). One hundred CHD patients were divided into the intervention (IG, AKO) and control (CG, placebo) groups. Before and after 1, 2, and 3 months of intervention, we measured serum levels of reactive oxygen species (ROS), 8-hydroxy-2-deoxyguanosine (8-OHdG), nitric oxide (NO), malondialdehyde (MDA), superoxide dismutase (SOD), reduced glutathione (GSH), and glutathione peroxidase (GPx), and KEAP1 and NRF2 levels in peripheral blood leukocytes (PBLs). Serum FAs were measured by GC at baseline and after 3-month intervention. RESULTS: AKO contains rich eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), which is more than 27% of total FA. The levels of EPA and DHA, KEAP1, and NRF2 in the IG group were higher than those in the CG group (p < 0.05). Serum levels of ROS, 8-OHdG, NO, and MDA in the IG group were lower than those in the CG group, whereas the levels of SOD, GSH, and GPx in the IG group were higher than those in the CG group (p < 0.05). Serum levels of saturated fatty acids (UFA) in the IG group were higher than those in the CG group, whereas reverse results were obtained for the levels of saturated fatty acids (SFA). Serum levels of EPA and DHA had a strong negative relationship with the level of ROS, whereas the ROS level had a strong negative relationship with the levels of KEAP1-NRF2. CONCLUSION: AKO increases antioxidant capacities of CHD patients via the KEAP1-NRF2 signaling in the PBL.

Identification of TNO155, an Allosteric SHP2 Inhibitor for the Treatment of Cancer.

SHP2 is a nonreceptor protein tyrosine phosphatase encoded by the PTPN11 gene and is involved in cell growth and differentiation via the MAPK signaling pathway. SHP2 also plays an important role in the programed cell death pathway (PD-1/PD-L1). As an oncoprotein as well as a potential immunomodulator, controlling SHP2 activity is of high therapeutic interest. As part of our comprehensive program targeting SHP2, we identified multiple allosteric binding modes of inhibition and optimized numerous chemical scaffolds in parallel. In this drug annotation report, we detail the identification and optimization of the pyrazine class of allosteric SHP2 inhibitors. Structure and property based drug design enabled the identification of protein-ligand interactions, potent cellular inhibition, control of physicochemical, pharmaceutical and selectivity properties, and potent in vivo antitumor activity. These studies culminated in the discovery of TNO155, (3S,4S)-8-(6-amino-5-((2-amino-3-chloropyridin-4-yl)thio)pyrazin-2-yl)-3-methyl-2-oxa-8-azaspiro[4.5]decan-4-amine (1), a highly potent, selective, orally efficacious, and first-in-class SHP2 inhibitor currently in clinical trials for cancer.

Identification of activated pathways in lung adenocarcinoma based on network strategy.

BACKGROUND: Lung adenocarcinoma has increased incidence over the past years and is the cause for almost 50% of deaths attributable to lung cancer. The objective of this paper is to identify activated pathways associated with lung adenocarcinoma based on gene co-expression network analysis. MATERIALS AND METHODS: Kyoto Encyclopedia of Genes and Genomes pathway analysis of dysregulated genes was performed based on Expression Analysis Systematic Explorer test to illuminate the biological pathways. Co-expression networks of lung adenocarcinoma in different tumor Stages (IA, IB, IIA, IIB, IIIA, IIIB, and IV) were constructed by Empirical Bayes approach to reweight gene pair scores. Pathway activity analysis was conducted to compute the distribution of pathways in different stages and to identify "activated" pathways in lung adenocarcinoma. RESULTS: We evaluated 211 dysregulated genes between lung adenocarcinoma patients and normal controls. Pathway activity analysis was performed and P values of pathways, which obtained from co-expression networks (Stage IA, IB, IIA, IIB, IIIA, IIIB, and IV), were calculated. Cell cycle, progesterone-mediated oocyte maturation, and oocyte meiosis were activated during all stages in lung adenocarcinoma. CONCLUSIONS: We successfully identified three activated pathways (cell cycle, progesterone-mediated oocyte maturation, and oocyte meiosis) in different Stages (IA, IB, IIA, IIB, IIIA, IIIB, and IV) of lung adenocarcinoma.

LIMD1-AS1 suppressed non-small cell lung cancer progression through stabilizing LIMD1 mRNA via hnRNP U.

BACKGROUND: Non-small cell lung cancer (NSCLC) occupies the majority of lung cancer cases and is notorious for the awful prognosis. LIM domains-containing 1 (LIMD1) is suggested as a tumor suppressor in lung cancer, but its mechanism in NSCLC remains elusive. Present study aimed to uncover the mechanism of LIMD1 in NSCLC. METHODS: qRT-PCR was performed to analyze the level of LIMD1. The functions of LIMD1 in NSCLC cells were evaluated by CCK-8, EdU, and caspase-3 activity assays. RIP and pull-down assays were applied to determine the interaction of LIMD1 with heterogeneous nuclear ribonucleoprotein U (hnRNP U) and LIMD1-AS1. RESULTS: LIMD1 was downregulated in NSCLC samples and cells. Functionally, LIMD1 hindered proliferation and drove apoptosis in NSCLC cells. Moreover, long noncoding RNA (lncRNA) LIMD1 antisense RNA 1 (LIMD1-AS1) was downregulated in NSCLC samples and cell lines. LIMD1-AS1 knockdown abrogated NSCLC cell growth in vitro and in vivo. Mechanistically, LIMD1-AS1 stabilized LIMD1 mRNA through interacting with hnRNP U. Rescue experiments suggested that LIMD1-AS1 repressed NSCLC progression through LIMD1. CONCLUSIONS: LIMD1-AS1 suppressed NSCLC progression through stabilizing LIMD1 mRNA via hnRNP U, providing new thoughts for the improvement of molecular-targeted therapy for NSCLC.

[Simulation model for cucumber growth and development in sunlight greenhouse]. / æ—¥å ‰æ¸©å®¤é»„ç“œç”Ÿé•¿å‘è‚²æ¨¡æ‹Ÿæ¨¡åž‹.

The dynamic simulation of cucumber growth and development in sunlight greenhouse can provide technical support for the intelligent management of cucumber production. According to the cucumber response characteristics to light and temperature, the cucumber development module based on the algorithm of clock model was established by using data from four-stage experiment with 'Jinyou 35' as experiment variety in two years. Based on the relationship between the leaf growth and key meteorological factors (temperature and radiation), leaf area index (LAI) module was established with the accumulated product of thermal effectiveness and photosynthetically active radiation (TEP) as independent variables. The simulation module of cucumber dry matter production was established by taking into consideration the double integral of LAI and daily length in photosynthesis per unit leaf area as well as the respiratory expenditure of different organs. Combined with water content of organs, fresh weight simulation module of cucumber organs was constructed. The whole cucumber development and growth simulation model in greenhouse was built based on each sub-module. The model parameters were calibrated and determined. The results showed that root mean square error (RMSE) of simulated values and observed values of four deve-lopment stages (from transplanting date to stretch tendril, to initial flowering, to early harvested and to uprooting), was 3.9-10.5 d. The normalized root mean square error (nRMSE) was 6.5%-28.6%. The coincidence index (D) was 0.79-0.97. The relationship between LAI and TEP was the regression of 'S' type curve. The RMSE of simulated and observed LAI values was 0.19. The nRMSE was 17.2%. The D value was 0.90. The RMSE of dry weight of root, stem, leaf, flower and fruit of the simulated values and observed values were 0.39-8.94 g·m-2. The nRMSE were 10.9%-17.7%. The D values were all above 0.98. The growth and development model of cucumber could accurately simulate the key development period of cucumber, leaf area and the dry and fresh weight of various organs and quantify the growth and development of cucumber in sunlight greenhouse.

Chain Extension and Synergistic Flame-Retardant Effect of Aromatic Schiff Base Diepoxide on Polyamide 6/Aluminum Diethylphosphinate Composites.

A way to suppress the deterioration in mechanical properties of polyamide 6 (PA6) is required, especially with high loading of flame retardants in the matrix. In this study, a novel aromatic Schiff base diepoxide (DES) was synthesized. It exhibited an efficient chain extension effect on PA6 and a synergistic flame-retardant effect with aluminum diethylphosphinate (AlPi) for PA6. The PA6 composite with 16 wt.% AlPi only passed UL-94 V-0 rating at 1.6 mm thickness, while the combination of 1.5 wt.% DES with 13 wt.% AlPi induced PA6 to achieve a UL-94 V-0 rating at 0.8 mm thickness. The tensile, flexural, and Izod notched impact strengths were increased by 16.2%, 16.5%, and 24.9%, respectively, compared with those of V-0 flame-retarded PA6 composites with 16 wt.% AlPi. The flame-retarded mechanism of PA6/AlPi/DES was investigated by cone calorimetry and infrared characterization of the char residues and pyrolysis products. These results showed that DES had a synergistic effect with AlPi in condensed-phase flame retardation by promoting the production of aluminum phosphorus oxides and polyphosphates in the char residues.

6-Amino-3-methylpyrimidinones as Potent, Selective, and Orally Efficacious SHP2 Inhibitors.

Protein tyrosine phosphatase SHP2 is an oncoprotein associated with cancer as well as a potential immune modulator because of its role in the programmed cell death PD-L1/PD-1 pathway. In the preceding manuscript, we described the optimization of a fused, bicyclic screening hit for potency, selectivity, and physicochemical properties in order to further expand the chemical diversity of allosteric SHP2 inhibitors. In this manuscript, we describe the further expansion of our approach, morphing the fused, bicyclic system into a novel monocyclic pyrimidinone scaffold through our understanding of SAR and use of structure-based design. These studies led to the identification of SHP394 (1), an orally efficacious inhibitor of SHP2, with high lipophilic efficiency, improved potency, and enhanced pharmacokinetic properties. We also report other pyrimidinone analogues with favorable pharmacokinetic and potency profiles. Overall, this work improves upon our previously described allosteric inhibitors and exemplifies and extends the range of permissible chemical templates that inhibit SHP2 via the allosteric mechanism.

Optimization of Fused Bicyclic Allosteric SHP2 Inhibitors.

SHP2 is a nonreceptor protein tyrosine phosphatase within the mitogen-activated protein kinase (MAPK) pathway controlling cell growth, differentiation, and oncogenic transformation. SHP2 also participates in the programed cell death pathway (PD-1/PD-L1) governing immune surveillance. Small-molecule inhibition of SHP2 has been widely investigated, including in our previous reports describing SHP099 (2), which binds to a tunnel-like allosteric binding site. To broaden our approach to allosteric inhibition of SHP2, we conducted additional hit finding, evaluation, and structure-based scaffold morphing. These studies, reported here in the first of two papers, led to the identification of multiple 5,6-fused bicyclic scaffolds that bind to the same allosteric tunnel as 2. We demonstrate the structural diversity permitted by the tunnel pharmacophore and culminated in the identification of pyrazolopyrimidinones (e.g., SHP389, 1) that modulate MAPK signaling in vivo. These studies also served as the basis for further scaffold morphing and optimization, detailed in the following manuscript.

A biobased Schiff base from protocatechualdehyde and its application in flame-retardant, low-smoke epoxy resin systems.

Herein, a new renewable Schiff base flame retardant 4,4'-((1E,1'E)-((oxybis(4,1-phenylene))bis(azanylylidene))bis(methanylylidene))bis(benzene-1,2-diol) (PH-ODA) was prepared by the reaction of protocatechualdehyde with 4,4'-diaminodiphenyl ether (ODA). PH-ODA (acting as a carbonization agent) combined with ammonium polyphosphate (APP) were used as intumescent flame retardants for commercial bisphenol A epoxy resin (DGEBA). For the cured epoxy resin containing 7.5% APP and 2.5% PH-ODA, the limiting oxygen index (LOI) reached 29.9% (with the V-0 rating in UL-94 test), and the peak heat release rate and total smoke production were respectively decreased by 88.1% and 68.3%, compared with pure epoxy resin. The enhancement of fire-safety performance was due to PH-ODA/APP promoting the formation of a compact intumescent char structure. It was also found that the synergism between PH-ODA and APP was helpful to enhance the fire resistance of the epoxy matrix. This work provides a facile and sustainable route for synthesizing Schiff base compounds from biomass-derived resources, possessing great potential for application in highly-effective intumescent flame retardants.

RETRACTED: Long non-coding RNA HULC promotes UVB-induced injury by up-regulation of BNIP3 in keratinocytes.

This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/our-business/policies/article-withdrawal). This article has been retracted at the request of the Editor-in-Chief. Concerns were raised about the background pattern of the Western Blots from Figures 4 and 5. Given the comments of Dr Elisabeth Bik regarding this article "This paper belongs to a set of over 400 papers (as per February 2020) that share very similar Western blots with tadpole-like shaped bands, the same background pattern, and striking similarities in title structures, paper layout, bar graph design, and - in a subset - flow cytometry panels", the journal requested the authors to provide the raw data. However, the authors were not able to fulfil this request and therefore the Editor-in-Chief decided to retract the article.

RETRACTED: Sinomenine inhibits lipopolysaccharide-induced inflammatory injury by regulation of miR-101/MKP-1/JNK pathway in keratinocyte cells.

This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/our-business/policies/article-withdrawal). This article has been retracted at the request of the Editor-in-Chief. Given the comments of Dr Elisabeth Bik regarding this article "This paper belongs to a set of over 400 papers (as per February 2020) that share very similar Western blots with tadpole-like shaped bands, the same background pattern, and striking similarities in title structures, paper layout, bar graph design, and - in a subset - flow cytometry panels", the journal requested the authors to provide the raw data. However, the authors were not able to fulfil this request and therefore the Editor-in-Chief decided to retract the article.

Allosteric inhibition of SHP2 phosphatase inhibits cancers driven by receptor tyrosine kinases.

The non-receptor protein tyrosine phosphatase SHP2, encoded by PTPN11, has an important role in signal transduction downstream of growth factor receptor signalling and was the first reported oncogenic tyrosine phosphatase. Activating mutations of SHP2 have been associated with developmental pathologies such as Noonan syndrome and are found in multiple cancer types, including leukaemia, lung and breast cancer and neuroblastoma. SHP2 is ubiquitously expressed and regulates cell survival and proliferation primarily through activation of the RAS­ERK signalling pathway. It is also a key mediator of the programmed cell death 1 (PD-1) and B- and T-lymphocyte attenuator (BTLA) immune checkpoint pathways. Reduction of SHP2 activity suppresses tumour cell growth and is a potential target of cancer therapy. Here we report the discovery of a highly potent (IC50 = 0.071 µM), selective and orally bioavailable small-molecule SHP2 inhibitor, SHP099, that stabilizes SHP2 in an auto-inhibited conformation. SHP099 concurrently binds to the interface of the N-terminal SH2, C-terminal SH2, and protein tyrosine phosphatase domains, thus inhibiting SHP2 activity through an allosteric mechanism. SHP099 suppresses RAS­ERK signalling to inhibit the proliferation of receptor-tyrosine-kinase-driven human cancer cells in vitro and is efficacious in mouse tumour xenograft models. Together, these data demonstrate that pharmacological inhibition of SHP2 is a valid therapeutic approach for the treatment of cancers.

Allosteric Inhibition of SHP2: Identification of a Potent, Selective, and Orally Efficacious Phosphatase Inhibitor.

SHP2 is a nonreceptor protein tyrosine phosphatase (PTP) encoded by the PTPN11 gene involved in cell growth and differentiation via the MAPK signaling pathway. SHP2 also purportedly plays an important role in the programmed cell death pathway (PD-1/PD-L1). Because it is an oncoprotein associated with multiple cancer-related diseases, as well as a potential immunomodulator, controlling SHP2 activity is of significant therapeutic interest. Recently in our laboratories, a small molecule inhibitor of SHP2 was identified as an allosteric modulator that stabilizes the autoinhibited conformation of SHP2. A high throughput screen was performed to identify progressable chemical matter, and X-ray crystallography revealed the location of binding in a previously undisclosed allosteric binding pocket. Structure-based drug design was employed to optimize for SHP2 inhibition, and several new protein-ligand interactions were characterized. These studies culminated in the discovery of 6-(4-amino-4-methylpiperidin-1-yl)-3-(2,3-dichlorophenyl)pyrazin-2-amine (SHP099, 1), a potent, selective, orally bioavailable, and efficacious SHP2 inhibitor.

Regional variations in the prevalence and misdiagnosis of air flow obstruction in China: baseline results from a prospective cohort of the China Kadoorie Biobank (CKB).

BACKGROUND: Despite the great burden of chronic respiratory diseases in China, few large multicentre, spirometry-based studies have examined its prevalence, rate of underdiagnosis regionally or the relevance of socioeconomic and lifestyle factors. METHODS: We analysed data from 512 891 adults in the China Kadoorie Biobank, recruited from 10 diverse regions of China during 2004-2008. Air flow obstruction (AFO) was defined by the lower limit of normal criteria based on spirometry-measured lung function. The prevalence of AFO was analysed by region, age, socioeconomic status, body mass index (BMI) and smoking history and compared with the prevalence of self-reported physician-diagnosed chronic bronchitis or emphysema (CB/E) and its symptoms. FINDINGS: The prevalence of AFO was 7.3% in men (range 2.5-18.2%) and 6.4% in women (1.5-18.5%). Higher prevalence of AFO was associated with older age (p<0.0001), lower income (p<0.0001), poor education (p<0.001), living in rural regions (p<0.001), those who started smoking before the age of 20 years (p<0.001) and low BMI (p<0.001). Compared with self-reported diagnosis of CB/E, 88.8% of AFO was underdiagnosed; underdiagnosis proportion was highest in 30-39-year olds (96.7%) compared with the 70+ age group (81.1%), in women (90.7%), in urban areas (89.4%), in people earning 5K-10 K ¥ monthly (90.3%) and in those with middle or high school education (92.6%). INTERPRETATION: In China, the burden of AFO based on spirometry was high and significantly greater than that estimated based on self-reported physician-diagnosed CB/E, especially in rural areas, reflecting major issues with diagnosis of AFO that will impact disease treatment and management.

Taiwanese parents' experience of making a "do not resuscitate" decision for their child in pediatric intensive care unit.

PURPOSE: The purpose of this project was to explore the parental experience of making a "do not resuscitate" (DNR) decision for their child who is or was cared for in a pediatric intensive care unit in Taiwan. METHODS: A descriptive qualitative study was conducted following parental signing of a standard hospital DNR form on behalf of their critically ill child. Sixteen Taiwanese parents of 11 children aged 1 month to 18 years were interviewed. Interviews were recorded, transcribed, analyzed and sorted into themes by the sole interviewer plus other researchers. RESULTS: Three major themes were identified: (a) "convincing points to sign", (b) "feelings immediately after signing", and (c) "post-signing relief or regret". Feelings following signing the DNR form were mixed and included "frustration", "guilt", and "conflicting hope". Parents adjusted their attitudes to thoughts such as "I have done my best," and "the child's life is beyond my control." Some parents whose child had died before the time of the interview expressed among other things "regret not having enough time to be with and talk to my child". CONCLUSION: Open family visiting hours plus staff sensitivity and communication skills training are needed. To help parents with this difficult signing process, nurses and other professionals in the pediatric intensive care unit need education on initiating the conversation, guiding the parents in expressing their fears, and providing continuing support to parents and children throughout the child's end of life process.

[Determination and clinical significance of serum surfactant proteins A and D in children with bronchiolitis].

OBJECTIVE: To study the variation and clinical significance of serum levels of surfactant proteins A (SP-A) and D (SP-D) among children with different degrees of bronchiolitis. METHODS: Seventy children with bronchiolitis were divided into acute (n=42) and recovery phase groups (n=28). According to the severity of symptoms, the acute phase group was further divided into severe (n=12) and mild subgroups (n=30). Another 26 children who were hospitalized in the same period due to non-infectious diseases and had not undergone surgery were used as the control group. Competitive enzyme-linked immunosorbent assay was performed to measure serum levels of SP-A and SP-D in each group. RESULTS: The acute phase group had significantly higher serum levels of SP-A and SP-D compared with the recovery phase (P<0.01) and control groups (P<0.01). Compared with the control group, the recovery phase group had elevated levels of SP-A and SP-D (P<0.01). Within the acute phase group, serum levels of SP-A and SP-D in the severe subgroup were significantly higher than in the mild subgroup (P<0.01). CONCLUSIONS: Serum levels of SP-A and SP-D are significantly elevated in children with acute bronchiolitis, and severe cases have higher serum levels of SP-A and SP-D than mild cases. Even after the relief of clinical symptoms, serum levels of SP-A and SP-D remain high. These findings suggest that serum levels of SP-A and SP-D might be useful biomarkers for evaluating the severity of bronchiolitis among children.