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This study aims to investigate the effects of Traditional Chinese medicine, Periplaneta americana extract (PAE), on osteoblast differentiation of human alveolar bone marrow-derived mesenchymal stem cells (hABMMSCs).hABMMSCs were treated with different concentrations of PAE. Cell Counting Kit-8 (CCK-8) assay and Transwell migration assay were conducted to evaluate cell proliferation and migration, respectively. Alkaline phosphatase (ALP) staining, ALP activity assay, and Alizarin red S staining were performed to detect osteogenesis in hABMMSCs. Additionally, real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot (WB) assay were performed to evaluate expression levels of osteogenic markers. Finally, RNA sequencing analysis and WB were carried out to elucidate the underlying mechanism.0.1 mg/ml PAE promoted cell proliferation and migration. PAE also increased ALP activity and mineralized nodule formation of hABMMSCs. In addition, PAE upregulated the expression of osteogenesis-related genes (RUNX2, COL1A1 and BGLAP). RNA-sequencing analysis revealed that PAE activated the focal adhesion signaling pathway. Treatment with Defactinib, an inhibitor of FAK, attenuated the effects induced by PAE.PAE could enhance osteoblast differentiation of hABMMSCs through focal adhesion signaling pathway, suggesting a therapeutic potential for alveolar bone defect.

The environmental certification acts as a sustainable practice for firms to improve their competitive advantage and its motivation has been widely discussed. However, existing researches ignore the important market driving force of green public procurement (GPP) as a policy tool. To fill this gap, this study, focusing on manufacturing firms in China and three typical environmental certifications, explores the relationship between GPP market pressure and firm's environmental certification practice based on institutional theory. Additionally, from a strategic perspective of green human resource management, this study unveils the influence mechanism of top management support in this relationship by using upper echelons theory. According to the empirical results, we find that GPP market pressure is positively associated with environmental certification practice, and top management support partially mediates this relationship. This study provides new insights into the explanation of firm's environmental certification practice, and provides practical implications for firm managers and government administrator.

Parkinson's disease (PD) is a neurodegenerative disease characterized by progressive loss of dopaminergic neurons in the substantia nigra and striatum. Glial cell line-derived neurotrophic factor (GDNF) can effectively promote the differentiation and survival of many types of neurons, especially dopaminergic neurons, suggesting it could be a treatment for PD. Lipid rafts are highly dynamic cell membrane domains that contain numerous signal protein receptors, providing an important platform for signal transduction. Compelling evidence indicates that alterations in lipid rafts are associated with PD, and some studies have reported that GDNF can regulate the expression of caveolin-1, a lipid raft-marker protein. However, the precise effects of GDNF on lipid rafts remain unknown. We developed a cellular PD model, purified detergent-resistant membranes (membrane rafts), and performed proteomic and lipid metabolomics analyses to examine changes in lipid rafts after GDNF treatment. The results showed considerable protein and lipid alterations in response to GDNF, especially altered levels of dopamine-β-hydroxylase, heat shock 70 kDa protein, neural cell adhesion molecule, cytoskeletal proteins, and long-chain polysaturated/unsaturated fatty acids. These findings reveal a new avenue to explore the relationships between GDNF, lipid rafts, and PD and support the hypothesis that GDNF may be a useful treatment for PD.

Although circulating tumor cells (CTCs) have shown promise as potential biomarkers for diagnostic and prognostic assessment in gastric cancer (GC), determining the predictive and prognostic value of programmed death‐ligand 1 (PD‐L1)‐positive CTCs in patients with GC is a challenge. Here, we identified that the expression of total vimentin (VIM) protein was positively correlated with PD‐L1 and inhibited CD8+ T‐cell activation in patients with GC according to bioinformatics analysis. Notably, coexpression of PD‐L1 and cell‐surface VIM (CSV) was detected by immunofluorescence and immunohistochemistry assay in locally advanced GC tumor specimens and metastatic lymph nodes. Likewise, CSV expression level was significantly decreased after transiently knocking down PD‐L1 in GC cell lines. Based on our established CTC detection platform, CTCs were isolated from peripheral blood samples collected from 70 patients (38 resectable and 32 unresectable) with GC using magnetic positive selection and a CSV‐specific monoclonal antibody, 84‐1. CSV+PD‐L1+CTCs were observed in 50 of 70 (71%) GC patient samples, ranging from 0 to 261 mL−1. A higher number of CSV+PD‐L1+CTCs were significantly associated with a short survival duration and poor therapeutic response. This study demonstrated that detection of PD‐L1+CTCs using a CSV‐enrichment method has promising value as a clinically relevant prognostic marker for GC., CSV+PD‐L1+CTC exhibits epithelial mesenchymal transition subtype, which can be observed in GC patient’s peripheral blood samples. A higher number of CSV+PD‐L1+CTCs are significantly associated with a short survival duration and poor therapeutic response.

The calculation of abutment stress has always been the most important topic in safe underground mining and design. In this paper, based on the formation mechanism of abutment stress, combined with the mechanical properties of actual strata and the theory of elastic foundation beams, a structure model of overlying strata with an elastic foundation is established, and a new theoretical calculation method of abutment stress is proposed. The new calculation method takes into account the interaction of the overlying key strata and the effect on the transmission of the front abutment stress and then analyzes the stress patterns of multilayered key strata under the combined action of the bending moment, shear force, and nonuniform load and its transmission to the underlying strata. In addition, based on field observations of panel 10 305 in the Xinglongzhuang coalmine, the influence range, peak position, and variation trend of the front abutment stress before and after breaking of the overlying key strata are studied and verified. The results show that the influence range of the abutment stress remains unchanged after KS1 breaks (eg, from 0 to 180 m), and its peak position shifts forward from 8 to 19 m, while the influence range (0‐180 m) and its peak position (6‐8 m in front of coal wall) remain unchanged after KS2 breaks; the abutment stress decreases, and the maximum decrease is 3.9 MPa in the range of 0‐22 m ahead of the coal wall after KS1 breaks, while the maximum decrease in the abutment stress is 2.1 MPa in the range of 0‐71 m ahead of the coal wall after KS2 breaks. The results of the new calculation method are basically consistent with the field observations and the existing theoretical results, showing that the method has good adaptability and reliability and can provide a new theoretical basis for on‐site design and construction practices.

The interaction between Axin and DVL2 is critical for the breaking down of the beta‐catenin destruction complex and the activation of the Wnt/beta‐catenin cascade. However, this biological process remains poorly understood. In the present study, TM4SF1 was identified as the interacting partner of DVL2 and positively regulated as Wnt/beta‐catenin signalling by strengthening the DVL2‐Axin interaction. The expression levels of TM4SF1 were elevated in hepatocellular carcinoma (HCC) and were induced by Kras signalling. The overexpression of TM4SF1 promoted the growth and motility of HCC cells, and up‐regulated the target genes (Axin2 and cyclin D1). The down‐regulation of TM4SF1 impaired the capability of HCC cells for growth, migration and metastasis. In addition, the down‐regulation of TM4SF1 promoted the ubiquitination of beta‐catenin. In summary, these results reveal the oncogenic functions of TM4SF1 in HCC progression and suggest that TM4SF1 might be a target for treatment.

Perylene derivatives can be stimulated by the hypoxic tumor microenvironment to generate radical anion that is proposed to arouse electron exchange with oxidizing substance, and in turn, realize reactive oxygen species (ROS) burst. Here, three perylene therapeutic agents, PDI-NI, PDIB-NI, and PDIC-NI, are developed and it is found that the minimum lowest unoccupied molecular orbital (LUMO) energy level makes PDIC-NI most easily accept electrons from the oxidative respiratory chain to form lots of anions, and the resultant maximum ROS generation, establishing an unambiguous mechanism for the formation of perylene radical anions in the cell, presents solid evidence for LUMO energy level determining endogenous ROS burst. Stirringly, PDIC-NI-induced ROS generation arouses enhanced mitochondrial oxidative stress and concurrently activates immunogenic cell death (ICD), which not only efficiently kills lung tumor cells but also reprograms immunosuppressive tumor microenvironment, including the cytokine secretion, dendritic cell maturation, as well as cytotoxic T lymphocytes activation, to inhibit the growth of xenografted and metastasis tumor, presenting a proof-of-concept demonstration of perylene that acts as an integrated therapeutic agent to well realize hypoxia-activated chemotherapy with ICD-induced immunotherapy on lung cancer.

Background Pathological and genetic evidence implicates toxic effects of aggregated α‐synuclein in the pathophysiology of neuronal dysfunction and degeneration in Parkinson's disease. Immunotherapy targeting aggregated α‐synuclein is a promising strategy for delaying disease progression. Objective This study (NCT02459886) evaluated the safety, tolerability, and pharmacokinetics of BIIB054, a human‐derived monoclonal antibody that preferentially binds to aggregated α‐synuclein, in healthy volunteers and participants with Parkinson's disease. Methods A total of 48 healthy volunteers (age 40–65, 19 women) and 18 Parkinson's disease participants (age 47–75, 5 women, Hoehn and Yahr stage ≤2.5) were in the study. Volunteers were enrolled into 6 single‐dose cohorts of BIIB054 (range 1–135 mg/kg) or placebo, administered intravenously; Parkinson's disease participants received a single dose of BIIB054 (15 or 45 mg/kg) or placebo. All participants were evaluated for 16 weeks with clinical, neuroimaging, electrocardiogram, and laboratory assessments. Serum and cerebrospinal fluid BIIB054 concentrations were measured. BIIB054/α‐synuclein complexes were measured in plasma. Results Most adverse events were mild and assessed by investigators as unrelated to the study drug. Pharmacokinetic parameters for volunteers and the Parkinson's disease participants were similar. BIIB054 serum exposure and maximum concentrations were dose proportional during the dose range studied. In volunteers and the Parkinson's disease participants, the serum half‐life of BIIB054 was 28 to 35 days; the cerebrospinal fluid–to‐serum ratio ranged from 0.13% to 0.56%. The presence of BIIB054/α‐synuclein complexes in plasma was confirmed; all Parkinson's disease participants showed almost complete saturation of the BIIB054/α‐synuclein complex formation. Conclusions BIIB054 has favorable safety, tolerability, and pharmacokinetic profiles in volunteers and Parkinson's disease participants, supporting further clinical development. © 2019 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.

Growth differentiation factor 11 (GDF11), a secreted member of the transforming growth factor-β (TGF-β) superfamily, has been reported to have the capacity to reverse age-related pathologic changes and regulate organ regeneration after injury; however, the role of GDF11 in fracture healing and bone repair is still unclear. Here, we established a fracture model in 12-week-old male mice to observe two healing states: the cartilaginous callus and bony callus formation phases. Our results showed that recombinant GDF11 (rGDF11) injection inhibits cartilaginous callus maturation and hard callus formation, thereby impairing fracture healing in vivo. In vitro, rGDF11 administration inhibited chondrocyte differentiation and maturation by phosphorylating SMAD2/3 protein and inhibiting RUNX2 expression. Notably, inhibition of TGF-β activity by a SMAD-specific inhibitor attenuated GDF11 effects. Thus, our study demonstrates that, rather than acting as a rejuvenating agent, rGDF11 impairs fracture healing by inhibiting chondrocyte differentiation and maturation.

Daytime radiative cooling serving as a method to pump heat from objects on Earth to cold outer space is an attractive cooling option that does not require any energy input. Among radiative cooler structures, the multilayer‐ or photonic‐structured radiative cooler, composed of inorganic materials, remains one of the most complicated structures to fabricate. In this study, transparent sapphire‐substrate‐based radiative coolers comprising a simple structure and selective emitter‐like optical characteristics are proposed. Utilizing the intrinsic optical properties of the sapphire substrate and adopting additional IR emissive layers, such as those composed of silicon nitride thin film or aluminum oxide nanoparticles, high‐performance radiative coolers can be fabricated with a low mean absorptivity (3–4%) at 0.3–2.5 µm and a high mean emissivity of over 90% at 8–13 µm. Experiments show that the fabricated radiative coolers reach temperature drops of ≈10 °C in the daytime. From the theoretical calculations of radiative cooling performance, the sapphire‐substrate‐based radiative coolers demonstrate a net cooling power as high as 100 Wm−2., Sapphire substrate‐based radiative coolers are introduced having simple structure and selective emitter‐like optical characteristics. Utilizing the intrinsic optical properties of sapphire substrate and additional IR emissive materials, high‐performance radiative coolers composed of purely inorganic materials are presented without elaborate simulation work previous studies reported.

New findings What is the central question of this study? Thoracic aortic aneurysm and dissection (TAAD) is characterized by extracellular matrix remodelling and an inflammatory response. Evidence suggests that ADAMTS1 is closely associated with TAAD development, but whether it contributes to the pathophysiology of TAAD remains unknown. What is the main finding and its importance? We generated inducible postnatal ADAMTS1 knockout mice and found that ADAMTS1 deficiency attenuated β-aminopropionitrile-dependent TAAD formation and rupture. Furthermore, ADAMTS1 deficiency suppressed neutrophil and macrophage infiltration by inhibiting inflammatory cytokine levels and macrophage migration during the early stage of β-aminopropionitrile-induced TAAD. ADAMTS1 could be a new therapeutic target for TAAD. Abstract Thoracic aortic aneurysm and dissection (TAAD), as a life-threatening cardiovascular disease, is characterized by extracellular matrix remodelling and an inflammatory response. A disintegrin and metalloproteinase with thrombospondin motifs 1 (ADAMTS1) is an inflammation-related protein that is able to degrade extracellular matrix proteins in arteries. Herein, we investigated whether ADAMTS1 contributes to the pathophysiology of TAAD in mice. Using the mouse model of β-aminopropionitrile (BAPN)-induced TAAD, we found that ADAMTS1 expression was upregulated beginning in the early stage of TAAD development and localized predominantly in the aortic adventitia. ADAMTS1-floxed mice and whole-body tamoxifen-inducible ADAMTS1 knockout mice (ADAMTS1flox/flox Ubc-CreERT2+ , ADAMTS1 KO) were generated to investigate the direct causal role of ADAMTS1 in TAAD development. The incidence and rupture rates of BAPN-induced TAAD in ADAMTS1 KO mice were significantly lower than those in ADAMTS1flox/flox mice (45.5 versus 81.8% and 18.2 versus 42.4%, respectively). Aortas from BAPN-treated ADAMTS1flox/flox mice displayed profound destruction of the elastic lamellae, abundant neutrophil and macrophage accumulation in the adventitia, obviously increased neutrophil proportions in peripheral blood and significantly increased expression of inflammatory factors in the early stage of TAAD induction, all of which were markedly suppressed in ADAMTS1 KO mice. Furthermore, ADAMTS1-deficient macrophages exhibited abrogated migration capacity both in vivo and in vitro. In conclusion, ADAMTS1 plays a crucial role in postnatal TAAD formation and rupture by regulating inflammatory responses, suggesting that ADAMTS1 might be a new therapeutic target for TAAD.

Transforming growth factor-β-induced (TGFΒI) is considered to be a vital gene in several carcinomas. In this study we determined the effect of TGFBI on the proliferative and metastatic potential of human urothelial carcinoma (UC) cells as well as its mRNA and protein expression, which were detected by RT-PCR and western blot, respectively. UC cell proliferation was analyzed by WST-1 assay and Hoechst 33258 staining. The effect of TGFBI on UC cell metastasis was analyzed using adhesion, migration and invasion assays. We found that TGFBI increased the proliferation of UC cells. Moreover, TGFBI enhanced the adhesion, migration and invasion of UC cells by upregulating MMP-2, MMP-9 and calpain-2 expression. We evaluated the effect of Epirubicin (EPI) on the regulation of TGFBI expression and found that TGFBI acts as a downstream target of EPI and is suppressed by EPI in UC cells. EPI is more effective in inhibiting the proliferation and metastasis of UC cells with high TGFBI expression. This study demonstrates that TGFBI might lead to tumorigenesis and progression of UC and those cells with high TGFBI expression may be vulnerable to relapse. EPI could prove to be a therapeutic option in patients with high TGFBI expressing UC cells.

We explored the role of microRNA‐30a (miR‐30a) and the mechanism involved in hepatic fibrosis. MiR‐30a overexpression was achieved by miR‐30a mimics transfection in hepatic stellate cells (HSCs) (HSC‐T6, LX‐2), and miR‐30a agomir (ago‐miR‐30a) treatment in mice. MiR‐30a levels were measured using TaqMan miRNA assay system, and the localization of miR‐30a was detected by fluorescence in situ hybridization (FISH). The interaction of miR‐30a and Beclin1 was confirmed by dual‐luciferase reporter assay. Autophagic flux was analysed using tandem mRFP‐GFP‐LC3 fluorescence microscopy, electron microscopy and Western blot of LC3‐II/I ratio. MiR‐30a was notably down‐regulated in activated HSCs and LX‐2‐exosomes induced by TGF‐β1; overexpression of miR‐30a down‐regulated extracellular matrix (ECM), such as α‐SMA, TIMP‐1, and Collagen I expression, and suppressed cell viability in HSCs. MiR‐30a was significantly down‐regulated in hepatic fibrosis mice and overexpression of miR‐30a prevented BDL‐induced fibrogenesis, concomitant with the down‐regulation of ECM. MiR‐30a inhibited HSCs autophagy and increased lipid accumulation in HSCs and in mice fibrotic hepatic tissues. MiR‐30a inhibited its downstream effector of Beclin1 by direct targeting its 3′‐UTR region. Moreover, Knock‐down of Beclin1 by small interfering RNA (siRNA) inhibited HSC autophagy and activation in LX‐2 cells. In conclusion, miR‐30a is down‐regulated in hepatic fibrosis models and its overexpression prevents liver fibrogenesis by directly suppressing Beclin1‐mediated autophagy; therefore, miR‐30a may be a new potential therapeutic target for controlling hepatic fibrosis.

Objectives Growth differentiation factor 11 (GDF11), an emerging secreted member of the TGF‐beta superfamily, plays essential roles in development, physiology and multiple diseases; however, its role during adipogenic differentiation and the underlying mechanisms remains poorly understood. Materials and methods Bone marrow‐derived human mesenchymal stem cells (hMSCs) and 3T3‐L1 pre‐adipocytes were induced with adipogenic culture medium supplementing with different concentrations of recombinant GDF11 (rGDF11 0, 10, 50, 100 ng mL−1). Oil Red O staining, qRT‐PCR analysis, Western blot analysis and immunofluorescence staining were performed to assay adipogenesis. Results For both hMSCs and 3T3‐L1 pre‐adipocytes, the presence of rGDF11 leads to a dose‐dependent reduction of intracellular lipid droplet accumulation and suppressed adipogenic‐related gene expression. Mechanically, GDF11 inhibits adipogenesis by activating Smad2/3‐dependent TGF‐beta signalling pathway, and these inhibitory effects could be restored by SB‐431542, a pharmacological TGF‐beta type I receptor inhibitor. Conclusions Taken together, our data indicates that GDF11 inhibits adipogenic differentiation in both hMSCs and 3T3‐L1 pre‐adipocytes by activating Smad2/3‐dependent TGF‐beta signalling pathway.

Polyphyllin VI (PVI) and polyphyllin VII (PVII) derived from Paris polyphylla possess anti-cancer activities. However, the mechanisms for the anti-lung cancer effects of PVI and PVII remain poorly understood. In this study, PVI and PVII exhibited inhibitory effects on the proliferation of A549 and NCI-H1299 cells. PVI and PVII induced G2/M cell cycle arrest and triggered apoptosis. PVI and PVII upregulated the tumor suppressor protein p53 and downregulated cyclin B1. The two treatments significantly increased the expression levels of death receptor 3, death receptor 5, Fas, cleaved PARP, and cleaved caspase-3. Furthermore, PVI and PVII significantly inhibited the growth of A549 cells in vivo. The tumor inhibitory rates of PVI were 25.74%, 34.62%, and 40.43% at 2, 3, and 4 mg/kg, respectively, and those of PVII were 25.63%, 41.71%, and 40.41% at 1, 2, and 3 mg/kg, respectively. Finally, PVI and PVII regulated the expression of proteins related to the apoptotic pathway in A549 xenografts. In summary, PVI and PVII exhibited strong inhibitory effects on lung cancer cell growth in vitro and in vivo by inducing G2/M cell cycle arrest and triggering apoptosis.

Since the turn of the millennium, an alternative type of magnetic sensor, based on the magneto-electric (ME) effect, has been widely investigated [1–5]. The ME effect is defined as a variation of dielectric po-larization in a material when subjected to an applied mag-netic field [6]. Previous reports indicated that the linear response of the ME sensor was the best [7, 8]. However, the linear response of ME composites is sensitive to the in-trinsic and extrinsic noises including the vibrational noise introduced via the piezoelectric effect and the intrinsic noise, such as Johnson noise, 1/

Objectives Lycoris is aurea agglutinin (LAA) has attracted rising attention due to its remarkable bioactivities. Here, we aimed at investigating its anti-tumor activities. Material and Methods In vitro methods including MTT, cellular morphology observation, FCM and immunoblotting were performed. In vivo methods like detection of tumor volume, body weight and survival ratio, as well as TUNEL staining were performed. Results and Conclusion LAA triggers G2/M phase cell cycle arrest via up-regulating p21expression as well as down-regulating cdk-1cyclinA singling pathway, and induces apoptotic cell death through inhibiting PI3K-Akt survival pathway in human lung adenocarcinoma A549 cells. While LAA has no significant cytotoxic effect toward normal human embryonic lung fibroblast HELF cells, and moreover, LAA could amplify the antineoplastic effects of cisplatin toward A549 cells. Lastly LAA also bears anti-cancer and apoptosis-inducing effects in vivo, and it could decrease the volume and weight of subcutaneous tumor mass obviously as well as expand lifespan of mice. These findings may provide a new perspective for elucidating the complicated molecular mechanisms of LAA-induced cancer cell growth-inhibition and death, providing a new opportunity of LAA as a potential candidate anti-neoplastic drug for future cancer therapeutics.

Aging behavior of Vectran fiber exposed to ultraviolet (UV) radiation was investigated. Vectran fiber was subjected to UV-accelerated degradation environment. Tensile strength of Vectran fiber was determined at room temperature using a two-parameter Weibull distribution. The average tensile strength loss was 42.75% when the irradiation time reached 186 h. The surface morphology of the degraded fiber was examined using scanning electron microscopy (SEM) and atomic force microscopy (AFM). X-ray photoelectron spectroscopy (XPS) and 13C-NMR were used to provide a molecular characterization of fibers. SEM and AFM showed that UV exposure result in microvoids on the surface of fibers. The results of the XPS and 13C-NMR indicated that the UV radiation could lead to chain scission of fiber surface layer. © 2011 Wiley Periodicals, Inc. J Appl Polym Sci, 2012

This study compared the effect of isoflurane or propofol anaesthesia on postoperative hepatocellular injury, liver function and pro-inflammatory cytokine concentrations in 60 cirrhotic patients, after partial hepatectomy using Pringle's manoeuvre. In the isoflurane group postoperatively, both mean (SD) aspartate aminotransferase (day 1: 197 (123) U.l -1 vs 261 (143) U.l -1 ; p = 0.01; day 3: 465 (258) U.l -1 vs 578 (311) U.l -1 ; p = 0.02) and alanine aminotransferase (day 1: 575 (312) U.l -1 vs 714 (434) U.l -1 ; p = 0.04 and day 3: 776 (443) U.l -1 vs 898 (746) U.l -1 ; p = 0.03) were significantly lower compared with the propofol group. Mean (SD) postoperative white cell count was significantly lower with isoflurane than propofol (day 1: 12 (4) × 10 3 .mm -1 vs 16 (4) × 10 3 .mm -1 ; p = 0.01 and day 3: 10 (6) × 10 3 .mm -1 ; vs 14 (4); p = 0.01). Tumour necrosis factor-α (day 1) and interleukin-1 (days 1 and 3) concentrations were significantly lower with isoflurane. Compared with propofol, isoflurane is associated with an attenuated postoperative inflammatory response and less postoperative hepatocellular injury in patients having this procedure.

2-Phenyl-1, 2, 3-triazole-4-formylhydrazine (2) was prepared by hydrazinolysis of the corresponding ester 1. Reaction of 2 with CS2/KOH gave the oxadiazole derivatives (3) which via Mannich reaction with different dialkyl amines furnished 3-N, N-dialkyl derivatives (4a–c). Also, condensation of 2 with appropriate aromatic acid in POCI3 yielded oxadiazole derivatives (5a–c), or with aldehydes and ketones afforded hydrazones (6a–c). Cyclization of (6a–c) with acetic anhydride gave the desired dihydroxadiazole derivatives (7a–c). On the other hand, reaction of dithiocarbazate (8) with hydrazine hydrate gave the corresponding triazole derivative (9) which on treatment with carboxylic acids in refluxing POCI3 yielded s-triazole [3, 4–b]-1, 3, 4-thiadiazole derivatives (10a–b). The structures of all the above compounds were confirmed by means of IR, 1H NMR, MS and elemental analysis.

Based on a large-scale household survey conducted in 2007, this article reports on poverty concentration and determinants in China's low-income neighbourhoods and social groups. Three types of neighbourhood are recognized: dilapidated inner-city neighbourhoods, declining workers' villages and urban villages. Respondents are grouped into four categories: working, laid-off/unemployed and retired urban residents, together with rural migrants. We first measure poverty concentration across different types of neighbourhood and different groups. The highest concentrations are found in dilapidated inner-city neighbourhoods and among the laid-off/unemployed. Mismatches are found between actual hardships, sense of deprivation and distribution of social welfare provision. Second, we examine poverty determinants. Variations in institutional protection and market remuneration are becoming equally important in predicting poverty generation, but are differently associated with it in the different neighbourhoods and groups. As China's urban economy is increasingly shaped by markets, the mechanism of market remuneration is becoming a more important determinant of poverty patterns, especially for people who are excluded from state institutions, notably laid-off workers and rural migrants.

Bruton's tyrosine kinase (BTK), a member of the TEC family of kinases, plays a crucial role in B-cell maturation and mast cell activation. Although the structures of the unphosphorylated mouse BTK kinase domain and the unphosphorylated and phosphorylated kinase domains of human ITK are known, understanding the kinase selectivity profiles of BTK inhibitors has been hampered by the lack of availability of a high resolution, ligand-bound BTK structure. Here, we report the crystal structures of the human BTK kinase domain bound to either Dasatinib (BMS-354825) at 1.9 A resolution or to 4-amino-5-(4-phenoxyphenyl)-7H-pyrrolospyrimidin- 7-yl-cyclopentane at 1.6 A resolution. This data provides information relevant to the development of small molecule inhibitors targeting BTK and the TEC family of nonreceptor tyrosine kinases. Analysis of the structural differences between the TEC and Src families of kinases near the Trp-Glu-Ile motif in the N-terminal region of the kinase domain suggests a mechanism of regulation of the TEC family members.

Since the 1990s, the introduction of a market economy and the process of rapid urbanization have been accompanied by a new urban poverty related to lay-offs and unemployment as well as by large-scale rural-urban migration, which is different from the traditional urban poverty of the 'Three Nos' (no relatives or dependants, no working capacity and no source of income). This article focuses on new urban poverty in China under market transition and discusses the causes of poverty creation. Instead of considering Chinese new urban poverty only as a result of market mechanisms, it argues that the state as the manipulator of institutions and policies does matter in the creation of new urban poverty, and that the cleavages between the old and new institutions further intensify it. Specifically, the following aspects of the creation of new urban poverty are examined in detail: the adjustment of industrial policy, the reform of state-owned enterprises, evolution of the household registration system, and the transformation of the welfare state. © The 2006 Author(s) Journal Compilation © 2006 Blackwell Publishing Ltd.

Characterization of the thermal properties of the surface and subsurface structures of the skin can reveal the degree of hydration, the rate of blood flow in near-surface micro- and macrovasculature, and other important physiological information of relevance to dermatological and overall health status. Here, a soft, stretchable thermal sensor, based on the so-called three omega (i.e., 3ω) method, is introduced for accurate characterization of the thermal conductivity and diffusivity of materials systems, such as the skin, which can be challenging to measure using established techniques. Experiments on skin at different body locations and under different physical states demonstrate the possibilities. Systematic studies establish the underlying principles of operation in these unusual systems, thereby allowing rational design and use, through combined investigations based on analytical modeling, experimental measurements, and finite element analysis. The findings create broad opportunities for 3ω methods in biology, with utility ranging from the integration with surgical tools or implantable devices to noninvasive uses in clinical diagnostics and therapeutics.

Classification of peripheral T-cell lymphomas based on morphological criteria can present problems due to overlap in histological features amongst the subtypes. An immunohistochemical study was designed to study the follicular dendritic cell patterns in 21 cases of peripheral T-cell lymphoma which had been classified using the updated Kiel classification. Three patterns of distribution were observed: 1 follicular dendritic cells not detected (3 cases); 2 follicular dendritic cells restricted to remnant follicle centres (7); 3 follicular dendritic cells present as an expanded network of cells exceeding the confines of germinal centres (11). Ten out of 11 angioimmunoblastic lymphomas showed an expanded network of follicular dendritic cells. The only negative case showed features which, on review, were in keeping with a pleomorphic, medium and large cell lymphoma showing an unusual proliferation of small venules. Other than angioimmunoblastic lymphomas, only one other case showed follicular dendritic cell hyperplasia. This was an unclassified peripheral T-cell lymphoma. We conclude that follicular dendritic cell hyperplasia may be used an an aid to diagnosis of the angioimmunoblastic type of peripheral T-cell lymphoma, and we recommend the routine staining of these cells in typing of T-cell lymphomas to facilitate comparison between centres.