Single-Molecule Traps in Covalent Organic Frameworks for Selective Capture of C2H2 from C2H4-Rich Gas Mixtures.

Removing trace amounts of acetylene (C2H2) from ethylene (C2H4)-rich gas mixtures is vital for the supply of high-purity C2H4 to the chemical industry and plastics sector. However, selective removal of C2H2 is challenging due to the similar physical and chemical properties of C2H2 and C2H4. Here, we report a "single-molecule trap" strategy that utilizes electrostatic interactions between the one-dimensional (1D) channel of a covalent organic framework (denoted as COF-1) and C2H2 molecules to massively enhance the adsorption selectivity toward C2H2 over C2H4. C2H2 molecules are immobilized via interactions with the O atom of C=O groups, the N atom of C≡N groups, and the H atom of phenyl groups in 1D channels of COF-1. Due to its exceptionally high affinity for C2H2, COF-1 delivered a remarkable C2H2 uptake of 7.97 cm3/g at 298 K and 0.01 bar, surpassing all reported COFs and many other state-of-the-art adsorbents under similar conditions. Further, COF-1 demonstrated outstanding performance for the separation of C2H2 and C2H4 in breakthrough experiments under dynamic conditions. COF-1 adsorbed C2H2 at a capacity of 0.17 cm3/g at 2,000 s/g when exposed to 0.5 ml/min C2H4-rich gas mixture (99% C2H4) at 298 K, directly producing high-purity C2H4 gas at a rate of 3.95 cm3/g. Computational simulations showed that the strong affinity between C2H2 and the single-molecule traps of COF-1 were responsible for the excellent separation performance. COF-1 is also robust, providing a promising new strategy for the efficient removal of trace amounts of C2H2 in practical C2H4 purification.

A family case report of parathyroid carcinoma associated with CDC73 mutation in hyperparathyroidism-jaw tumor syndrome.

Background: Hereditary primary hyperparathyroidism (PHPT) accounts for 5-10% of all PHPT cases, necessitating genetic testing for diagnosis and management. Among these, hyperparathyroidism-jaw tumor syndrome (HPT-JT) is an autosomal dominant disorder caused by CDC73 mutations with variable clinical presentations and incomplete symptoms. Case summary: The proband, diagnosed with PHPT, underwent parathyroidectomy at the age of 41 with pathological examination of parathyroid carcinoma (PC). Hereditary PHPT was initially suspected due to the early-onset PHPT and family history. Genetic testing identified a heterozygous CDC73 mutation, NM_024529.4: c. 687_688delAG (p. Arg229Serfs*37). Even in the absence of jaw tumors, the diagnosis of HPT-JT was confirmed based on the discovery of renal cysts. A secondary thyroidectomy was performed to reduce the risk of recurrence. Conclusion: Genetic testing is strongly recommended in cases of early-onset PHPT, family history, jaw tumors, renal and uterine involvement, atypical parathyroid tumors, and PC. This testing provides valuable information for personalized management, and counseling is available for affected families.

Functionalized Iron-Nitrogen-Carbon Electrocatalyst Provides a Reversible Electron Transfer Platform for Efficient Uranium Extraction from Seawater.

Uranium extraction from seawater provides an opportunity for sustainable fuel supply to nuclear power plants. Herein, an adsorption-electrocatalysis strategy is demonstrated for efficient uranium extraction from seawater using a functionalized iron-nitrogen-carbon (Fe-Nx -C-R) catalyst, comprising N-doped carbon capsules supporting FeNx single-atom sites and surface chelating amidoxime groups (R). The amidoxime groups bring hydrophilicity to the adsorbent and offer surface-specific binding sites for UO2 2+ capture. The site-isolated FeNx centres reduce adsorbed UO2 2+ to UO2 + . Subsequently, through electrochemical reduction of the FeNx sites, unstable U(V) ions are reoxidized to U(VI) in the presence of Na+ resulting in the generation of solid Na2 O(UO3 ·H2 O)x , which can easily be collected. Fe-Nx -C-R reduced the uranium concentration in seawater from ≈3.5 ppb to below 0.5 ppb with a calculated capacity of ≈1.2 mg g-1 within 24 h. To the best of the knowledge, the developed system is the first to use the adsorption of uranyl ions and electrodeposition of solid Na2 O(UO3 .H2 O)x for the extraction of uranium from seawater. The important discoveries guide technology development for the efficient extraction of uranium from seawater.

Knockdown of IRE1ɑ suppresses metastatic potential of colon cancer cells through inhibiting FN1-Src/FAK-GTPases signaling.

The inositol-requiring enzyme 1α (IRE1α) is an endoplasmic reticulum (ER)-resident transmembrane protein and senses cellular unfolded/misfolded proteins. Upon activation, IRE1α removes a 26-bp nucleotide from the mRNA encoding X-box binding protein (XBP) 1 to generate a spliced active form of this transcription factor (XBP1s). Though IRE1α is implicated in development of cancer, the role and underlying mechanism remain unclear. Here, we demonstrate that IRE1α regulates colon cancer cell metastasis through regulating the expression of fibronectin-1 (FN1). We found that knockdown of IRE1α inhibited colon cancer cell migration and invasion in vitro and metastasis in vivo. Knockdown of IRE1α decreased the formation of XBP1s and attenuated the expression of FN1, leading to inhibition of phosphorylation of Src and FAK and inactivation the downstream effector GTPases including RhoA, Rac1 and CDC42. Addition of exogenous FN1 reversed Src/FAK phosphorylation and cell migration inhibited by IRE1α knockdown. We found that XBP1s bound FN1 promoter and acted as a transcription factor to initiate FN1 expression. Our results suggest that IRE1α modulates metastatic potential of colon cancer cells through regulating the expression of FN1.

Prolyl hydroxylase 2 is dispensable for homeostasis of intestinal epithelium in mice.

Prolyl hydroxylases (PHD1-3) hydroxylate hypoxia inducible factor α (HIFα), leading to HIFα ubiquitination and degradation. Recent studies indicated that administration of generic inhibitors of PHDs improved mice colitis, suggesting that suppression of PHD activity by these inhibitors may be a potential strategy for the treatment of inflammatory bowel diseases. However, the exact role of each member of PHD family in homeostasis of intestinal epithelium remains elusive. The aim of this work is to study the possible role of PHD2 by using mice with genetic ablation of Phd2 in intestinal epithelial cells (IECs). We found that deletion of PHD2 in IECs did not lead to spontaneous enteritis or colitis in mice. Deletion of PHD2 in IECs did not confer upon mice higher susceptibility to dextran sodium sulfate-induced colitis. Furthermore, in a colitis-associated colon cancer model, the PHD2-conditional knockout mice had similar susceptibility to azoxymethane (AOM)-induced colonic tumorigenesis as control mice did. Our results suggest that PHD2 is dispensable for maintenance of intestinal epithelium homeostasis in mice.

[A relationship between cyclooxygenase-2 expression and tumor angiogenesis in experimental rat liver carcinogenesis].

OBJECTIVE: To explore the relationship between the expression of cyclooxygenase-2 (COX-2) and angiogenesis in hepatocellular carcinoma. METHODS: Forty Wistar rats were divided into two groups: a model group (30 rats) and a normal group (10 rats). Hepatocellular carcinoma was induced with 0.01% diethylnitrosamine (DEN) in the model group rats. The rats were sacrificed in batches at the 6th, 12th and 18th week of the experiment. Histological sections of liver tissues were made using routine methods. The expressions of COX-2, VEGF, VEGFR-2/KDR, and MMP-2 protein in the liver tissues were evaluated using immunohistochemical methods. RESULTS: In liver sections from the model group there were marked pathological changes (steatosis, cell infiltration, cirrhosis and liver cancer). The expressions of VEGF, VEGFR-2/KDR, and MMP-2 in those liver tissues were remarkably increased during the hepatocellular carcinogenesis. Microvessel density (MVD) was also obviously raised during the process of the cancer development. There was a direct correlation between the MVD and VEGF/KDR/MMP-2 (r=0.858, 0.788, 0.684, respectively; all P less than 0.01). There was also a direct correlation between the COX-2 and VEGF/KDR/MMP-2/MVD (r=0.771, 0.599, 0.690, 0.788, respectively; all P < 0.01). CONCLUSION: COX-2 can promote tumor angiogenesis during rat hepatocellular carcinogenesis. This may be one of the mechanisms in which COX-2 promotes carcinomas.