Solvent-Free DABCO-Mediated [3 + 2] Cycloadditions of Donor–Acceptor Cyclopropanes with Aldehydes: Strategy for Synthesis of Fully Substituted Furans

DABCO-mediated [3 + 2] cycloadditions of donor–acceptor cyclopropanes with aldehydes under solvent-free conditions have been developed for the preparation of fully substituted furans which are a wide range of structurally interesting and pharmacologically significant compounds. The reaction appears to be general for a variety of 1-cyano­cyclo­propane-1-carboxylates and aldehydes and tolerates the presence of aromatic moieties with electron-withdrawing and electron-donating substituents

The role of MALAT-1 in the invasion and metastasis of gastric cancer

<p><b>Objectives:</b> The long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT-1) has been reported to be over-expressed in several cancer types. However, its role in gastric cancer (GC) remains unclear. In the present study, we examined the expression of MALAT-1 in GC cells and tissues and explored its role in GC cell migration and invasion.</p> <p><b>Materials and methods:</b> Real-time quantitative polymerase chain reaction (qRT-PCR) was used to analyze the expression level of MALAT-1 in six GC cell lines and 20 gastric tissues (20 GC and 20 adjacent normal mucosa). Functional characterization for the role of MALAT-1 in GC was performed by small interfering RNA (siRNA) knockdown, followed by series of <i>in vitro</i> and <i>in vivo</i> experiments.</p> <p><b>Results:</b> MALAT-1 was upregulated in GC cell lines and tissues compared with the immortalized gastric epithelial cell line GES and adjacent normal tissues, respectively. Moreover, MALAT-1 expression was higher in the high-metastatic-potential GC cell line SGC7901M than in the low-metastatic-potential GC cell line SGC7901NM. <i>In vitro</i> and <i>in vivo</i> assays showed that siRNA-mediated silencing of MALAT-1 inhibited GC cell migration and invasion. In addition, suppressing MALAT-1 expression resulted in a decrease in the expression of the Epithelial-mesenchymal transition (EMT)-associated marker vimentin and an increase in the expression of E-cadherin at both the mRNA and protein levels.</p> <p><b>Conclusions:</b> MALAT-1 may promote the migration and invasion of GC cells in part by regulating EMT.</p

Carbon-Based CsPbBr₃ Perovskite Solar Cells: All-Ambient Processes and High Thermal Stability

The device instability has been an important issue for hybrid organic–inorganic halide perovskite solar cells (PSCs). This work intends to address this issue by exploiting inorganic perovskite (CsPbBr₃) as light absorber, accompanied by replacing organic hole transport materials (HTM) and the metal electrode with a carbon electrode. All the fabrication processes (including those for CsPbBr₃ and the carbon electrode) in the PSCs are conducted in ambient atmosphere. Through a systematical optimization on the fabrication processes of CsPbBr₃ film, carbon-based PSCs (C-PSCs) obtained the highest power conversion efficiency (PCE) of about 5.0%, a relatively high value for inorganic perovskite-based PSCs. More importantly, after storage for 250 h at 80 °C, only 11.7% loss in PCE is observed for CsPbBr₃ C-PSCs, significantly lower than that for popular CH₃NH₃PbI₃ C-PSCs (59.0%) and other reported PSCs, which indicated a promising thermal stability of CsPbBr₃ C-PSCs

Pharmacological inhibitors of JAK, PI3K/Akt, and MEK/ERK1/2 prevent NP cells growth from leptin induction.

<p>After 1-day serum deprivation, NP cell were treated vehicle (control), 10 ng/ml leptin (Lep), 40 µM AG490 (AG), 250 nM wortmannin (Wort), 10 µM U0126 (U0126), or 10 ng/ml leptin together with 40 µM AG490 (Lep+AG), 250 nM wortmannin (Lep+Wort), 10 µM U0126 (Lep+U0126), 40 µM AG490 and 10 µM U0126 (Lep +U0126+ AG), 40 µM AG490 and 250 nM wortmannin (Lep+AG+Wort), 10 µM U0126 and 250 nM wortmannin (Lep+U0126+Wort), 10 µM U0126, 40 µM AG490 and 250 nM wortmannin (Lep+U0126+ Wort+AG) in serum-free medium for 48 h. Values are presented as mean ±SD (n = 4). The statistically differences compared with the control are noted as *p<0.05, and ***p<0.001. Data represent three independent experiments.</p

Malformations in the limbs, pelvic and sacral of VAD neonates.

<p>(A) Side view of the forelimb region showing normal forelimb development in a control fetus. (B) VAD fetus showing deformities of ulna, at least unilaterally, in the forelimb region. (C) Ventral view of the pelvic region of a control fetus depicting normal development and attachment of the pelvic. (D) VAD fetus showing moderately dysplasia of the ischium. (E) Ventral view of the hindlimb region showing normal hindlimb development in a control fetus. (F) VAD fetus showing malformations of the tibia and fibula as well as tibia and fibula fusion. (G) Ventral view of the ossification region showing normal ossification development in a control fetus. (H) VAD fetus, the ossification of the second phalange was either missing or greatly reduced in size.</p

Characters of filial rats of VAD group and control group.

<p>Characters of filial rats of VAD group and control group.</p

Nucleotide sequences of primers used in Real-time RT-PCR.

<p>Nucleotide sequences of primers used in Real-time RT-PCR.</p

Malformations in the cervical and thoracic regions of VAD neonates.

<p>(A) Side view of cervical region showing normal skeletal in a control fetus. (B) VAD fetus showing loss of the neural arch in cervical 1. (C) Ventral view of the scapula region showing normal development in a control fetus. (D) VAD fetus showing dysplasias of the scapula. (E) Side view of the sternal elements showing normal development the manubrium, sternebrae and xyphoid process in a control fetus. (F) VAD fetus showing malformation of the sternal elements as well as loss of xyphoid process. (G) Ventral view of the thoraric region showing normal development in a control fetus. (H) VAD fetus showing anomalies of vertebrae in thoraric region as well as rib fusions. (I) Ventral view of the thoraric region showing normal development in a control fetus. (J) VAD fetus showing loss of rib in vertebral 20.</p

Transcription levels of retinaldehyde dehydrogenase (RALDH1, RALDH2 and RALDH3) and retinoid acid receptors (RARα, RARβ, RARγ) in the liver of control, VAD rat.

<p>Bar Mean ±SE of three samples in triplicate. *P<0.05 **P<0.01. VAD group VS Control group.</p

Representative anteropoterior radiographs showing no vertabral anomalies (Control Group) and with congential spinal deformities (VAD Group) original magnification ×2.

<p>Representative anteropoterior radiographs showing no vertabral anomalies (Control Group) and with congential spinal deformities (VAD Group) original magnification ×2.</p