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Intestinal ischemia-reperfusion (II/R) injury is a common clinical and pathological change; however, its underlying mechanisms remain unclear. Previous studies have shown that the inflammatory response induced by mast cell degranulation may be involved in the mechanism underlying II/R injury in rats. In this study, we established a human intestinal epithelial adenocarcinoma cell (Caco-2) hypoxia/reoxygenation (H/R) model and transwell system to investigate the effects of culture media (CM) from hypoxia conditioned human mast cell (HMC-1) and HMC-1 H/R on hypoxia/reoxygenation injury in Caco-2 under H/R conditions. Moreover, we assessed the barrier function of Caco-2 by measuring the 4-kDa fluorescein isothiocyanate (FITC)-dextran (FD4) flux and the tight junction protein expression. The results concluded that Caco-2 exposed to H/R insult showed an increase in lactate dehydrogenase (LDH) release, cell apoptosis index, cell permeability, Bax expression, phosphorylation of c-Jun N-terminal protein kinase (JNK) and p38, and a decrease in cell viability and expression of Bcl-2, ZO1, and occludin (all P < 0.05). Notably, preincubating Caco-2 with HMC-1CM resulted in an increase in cell injury (increased LDH levels and cell permeability, decreased cell viability), apoptosis index, p-JNK, and p-38 expression and a decrease in ZO1 and occludin expression by co-culture system (all P < 0.05). In conclusion, our results show that HMC-1 hypoxic and reoxygenated CM aggravates hypoxic and reoxygenated injury in Caco-2 by increasing the phosphorylation of JNK and p38 in vitro., Competing Interests: Conflicts of Interest The authors declare no competing financial interests., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

Rationale : Peripheral nerve block is a traditional perioperative analgesic method for its precise pain control and low systemic toxicity. However, a single low dose of local anesthetic merely provides a few hours of analgesia, and high dose results in irreversible toxicity, whereas continuous infusion of anesthetics is expensive and complicated. Therefore, it is necessary to develop a long-acting and sensory-selective local anesthetic for safe perioperative analgesia. Methods : An injectable composite comprising ropivacaine-loaded poly (ε-caprolactone) electrospun fiber and clonidine-loaded F127 hydrogel (Fiber-Rop/Gel-Clo composite) was developed for long-acting and walking regional analgesia with barely one dose. The peripheral nerve blockade effect of the composite was evaluated in a rat sciatic nerve block model. Also, the biodegradability and biosafety of the composite was evaluated. Results : The preferentially released Clo from the hydrogel rapidly constricted the peripheral arterial vessels, reducing the blood absorption of Rop and thus enhancing the local Rop accumulation at the injection site. The subsequently sustainable release of Rop from the fiber, significantly prolonged the sciatic nerve block of rats. Remarkably, an amazing sensorimotor segregation effect was achieved, as the sensory blockade (32.0 ± 1.4 h) lasted significantly longer than the motor blockade (20.3 ± 0.9 h). Additionally, the Fiber-Rop/Gel-Clo composite presented good biodegradability and biosafety in vivo . Conclusions : Our designed Fiber-Rop/Gel-Clo composite with minimal invasion, prolonged synergistic analgesia, and strikingly sensorimotor segregation effect, posted a promising prospect for regional long-term walking analgesia in clinical treatment., Competing Interests: Competing Interests: The authors have declared that no competing interest exists., (© The author(s).)

A series of C -functionalized β-ketoimine compounds at the terminal methyl groups of the β-ketoimine precursor L ph H 2 (L ph = C 6 H 4 [NC(Me)CHC(Me)O] 2 ) were prepared. This convenient transformation was realized via straightforward double alkylation on the terminal C α of a novel bis-dianionic β-ketoiminate lithium complex [L ph' Li 4 (THF) 4 ] 2 (L ph' = C 6 H 4 [NC(Me)CHC(O)CH 2 ] 2 ) followed by hydrolysis.

Circular RNAs (CircRNAs) were reported to play vital roles in the progression of DN. Herein, the action of circular RNA&#95;0037128 (circ&#95;0037128) was investigated in DN. The level of circ&#95;0037128, microRNA-497-5p (miR-497-5p) and nuclear factor of activated T cells 5 (NFAT5) was determined using quantitative real-time polymerase chain reaction (qRT-PCR). The feature of circ&#95;0037128 was tested by RNase R and Actinomycin D treatment assays. Cell Counting Kit-8 (CCK-8) and 5-ethynyl-2'-deoxyuridine (EdU) staining assays were conducted to evaluate the proliferation ability. The relative protein expression was determined via Western blot analysis. Levels of the inflammatory cytokines, like tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6), were assessed by enzyme-linked immunosorbent assay (ELISA). Reactive oxygen species (ROS) production, lactate dehydrogenase (LDH) and superoxide dismutase (SOD) activity were determined by the matched kits. Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays were conducted for evaluating the correlation between miR-497-5p and circ&#95;0037128 or NFAT5. Circ&#95;0037128 and NFAT5 were enhanced, while miR-497-5p was weakened in kidney tissues of DN patients and high glucose (HG)-cultured HK-2 cells. Circ&#95;0037128 inhibition bated HG-caused inhibition effect on cell proliferation and promotion effects on oxidative stress, inflammation and fibrosis in HK-2 cells. Moreover, circ&#95;0037128 knockdown alleviated HG-caused cell damage via regulating miR-497-5p. In addition, NFAT5 overexpression could reverse the influence of miR-497-5p on HG-induced injury in HK-2 cells. Mechanically, circ&#95;0037128 sponged miR-497-5p to modulate NFAT5. Circ&#95;0037128 downregulation could mitigate HG-stimulated cell damage via regulating the miR-497-5p/NFAT5 axis in HK-2 cells in vitro , providing a possible therapy target for DN.

Danxia landform occurring sporadically in southern China is a unique type of petrographic geomorphology. It has nurtured about 400 rare or threatened plant and animal species, whose diversity, endemism, and conservation have called increasing scientific and public attentions. Among them, Primulina danxiaensis (W. B. Liao, S. S. Lin, and R. J. Shen) W. B. Liao and K. F. Chung is a tiny perennial grass species recorded only in Mount Danxia, a natural World Heritage Site as part of China's Danxia. In this study, restriction site-associated DNA sequencing (RAD-seq) was performed to investigate genetic diversity among these 12 populations of P. danxiaensis . A total of 432,041 variant sites were detected in 84,779 loci across 94 samples. The expected heterozygosity ( H E ) ranged from 0.017 to 0.139. Bottleneck signals were detected in most populations, Tajima's D tests showed that most loci could be under recent positive selection, and one of the six positively selected loci identified by BayeScan was annotated as tRNA Glu , which may contribute to the species' adaptation to shady environment. STRUCTURE analysis and phylogenetic tree showed that the 12 populations of P. danxiaensis could be divided into four gene pools (clades) corresponding to their geographic locations, and significant correlation was observed between genetic and geographic distances. Our study demonstrated that P. danxiaensis maintained a middle level of genetic diversity and strong population structure; geographic distance could be an important factor limiting gene flow among populations of P. danxiaensis , which were only sporadically recorded in Mount Danxia., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Chen, Guo, Chen, Liao and Fan.)

Currently, only 5% of thermoset carbon fiber reinforced polymer composites (CFRPs) are recycled into lower-value secondary products. Highly efficient closed-loop recycling of both thermoset resin and carbon fiber is a major challenge. Here, we report a sustainable approach for the closed-loop recycling of the resin and fiber from CFRPs. Thiol-functionalized carbon fiber (TCF) obtained by functionalization with a thiol-ended hyperbranched polymer, and then an epoxy-ended degradable hyperbranched polymer (HT 3 ) are used to prepare HT 3 /TCF composites, which show considerable acid resistance and mechanical performance. The cured composites are controllably depolymerized into monomers and oligomers with high recyclability (89%), which can be utilized to prepare HT 3 and the precursor of cross-linked HT 3 . A total of 100% of the carbon fibers are recovered and reused to fabricate composites without deterioration of performance. The results provide a method for designing high-performance composites and a pathway for high efficiency closed-loop recycling.

Background: Epidemiological studies have shown that exposure to ambient fine particulate matter with aerodynamic diameter less than or equal to 2.5 μm ( PM 2.5 ) correlates with a decrease in sperm count, but the biological mechanism remains elusive., Objectives: This study tested whether hypothalamic inflammation, an emerging pathophysiological mediator, mediates the development of lower epididymal sperm count due to PM 2.5 exposure., Methods: Inhibitor κ B kinase 2 (IKK2) was conditionally knocked out either in all neurons or subtypes of hypothalamic neurons of mice. Effects of concentrated ambient PM 2.5 (CAP) exposure on hypothalamic inflammation, the hypothalamic-pituitary-gonadal (HPG) axis, and epididymal sperm count of these mouse models were then assessed. Furthermore, to test whether hypothalamic inflammation is sufficient to decrease sperm production, we overexpressed constitutively active IKK2 (IKK2ca) either in all neurons or subtypes of hypothalamic neurons and assessed hypothalamic inflammation, the HPG axis, and sperm production of these overexpression mouse models., Results: CAP-exposed wild-type control mice vs. filtered air (FA)-exposed wild-type control mice had a higher expression of hypothalamic inflammatory markers, lower functional indexes of the HPG axis, and a lower epididymal sperm count. In contrast, all these measurements for CAP- vs. FA-exposed mice deficient of IKK2 in all neurons were comparable. We also found that overexpression of IKK2ca in either all neurons or pro-opiomelanocortin (POMC) neurons only, but not in Agouti-related protein (AgRP) neurons only, resulted in lower functional indexes of the HPG axis and a lower epididymal sperm count. Moreover, we showed that CAP- vs. FA-exposed mice deficient of IKK2 in POMC neurons had a comparable expression of hypothalamic inflammatory markers, comparable functional indexes of the HPG axis, and a comparable epididymal sperm count., Discussion: This mouse model study shows a causal role of IKK2 of POMC neurons in the development of lower epididymal sperm count due to PM 2.5 exposure, providing a mechanistic insight into this emerging pathogenesis. https://doi.org/10.1289/EHP8868.

Considerable studies show that maternal exposure to ambient fine particulate matter (PM 2.5 ) programs offspring's susceptibility to obesity. However, few studies have investigated the effect of paternal PM 2.5 exposure on offspring's energy homeostasis. This study thus tested whether paternal PM 2.5 exposure programs offspring's energy homeostasis. Male C57Bl/6J mice were exposed to filtered air or concentrated ambient PM 2.5 (CAP) for 12 weeks and then mated with normal female C57Bl/6J mice. The offspring were assessed for growth trajectories, food intakes, and body compositions, and the sperm miRNAs of those sires were profiled by microarray. Zygotic injection was used to test whether the miRNA identified by the microarray mediates the impact of paternal PM 2.5 exposure on offspring's energy homeostasis. Paternal CAP exposure resulted in significant hypophagia and weight loss in male, but not female, offspring. The weight loss of male offspring was accompanied by decreases in the liver and kidney masses and paradoxically an increase in the adipose mass. Without further exposure to CAP, this programming was three-generationally transmitted along the paternal line. The sperm miRNA profiling revealed that mmu-mir6909-5p was the sole differentially expressed sperm miRNA due to PM 2.5 exposure, and zygotic injection of mmu-mir6909-5p mimicked all the effects of paternal PM 2.5 exposure on offspring's energy homeostasis. Paternal PM 2.5 exposure programs offspring's energy homeostasis through increasing paternal sperm mmu-mir6909-5p.

The genetic association of primary biliary cholangitis with major histocompatibility complex (MHC) has been widely confirmed among different ethnicities. To map specific MHC region variants associated with PBC in a Han Chinese cohort, we imputed HLA antigens and amino acids (AA) in 1126 PBC cases and 1770 healthy control subjects using a Han-MHC reference database. We demonstrate that HLA-DRB1 and/or HLA-DQB1 contributed the strongest signals, and that HLA-DPB1 was a separate independent locus. Regression analyses with classical HLA alleles indicate that HLA-DQB1*03:01 or HLA-DQβ1-Pro55, HLA-DPB1*17:01 or HLA-DPβ1-Asp84 and HLA-DRB1*08:03 could largely explain MHC association with PBC. Forward stepwise regression analyses with HLA amino acid variants localize the major signals to HLA-DRβ1-Ala74, HLA-DQβ1-Pro55 and HLA-DPβ1-Asp84. Electrostatic potential calculations implicated AA variations at HLA-DQβ1 position 55 and HLA-DPβ1 position 84 as critical to peptide binding properties. Furthermore, although several critical Han Chinese AA variants differed from those shown in European populations, the predicted effects on antigen binding are likely to be very similar or identical and underlie the major component of MHC association with PBC., (Copyright © 2019 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Rhodoleia Champion ex Hooker is one of the most primitive relict genera of Hamamelidaceae, a key family exploited to understand the origin and early evolution of flowering plants. Genomic simple sequence repeats (SSRs) were developed for R. championii to perform genetic diversity, phylogeographical structure or even systematic evolution studies of the genus. Among the 278,743 contigs (105,758,242 bps) de novo assembled from the low-coverage whole genome sequencing of R. championii, a total of 9106 SSRs were detected in 8370 contigs, and SSR primer pairs were successfully designed for 6677 SSRs. Among the 110 selected primer pairs, 41 were amplified successfully in the preliminary test of SSR screening. Further amplification of these 41 primer pairs across the 122 individuals collected from six populations of the three Rhodoleia species showed that 32 and 40 SSR markers can be amplified in Vietnam and Jinping populations of R. parvipetala, 41, 33, and 41 SSR markers in Boluo, Hongkong and Xinyi populations of R. championii, 25 SSR markers in Fugong population of R. forrestii, and 20 SSR markers demonstrated to be polymorphic across the three species. Genetic analysis for these 20 polymorphic SSRs showed that Allele number (A) ranged from four to 13 and polymorphic information content (PIC) ranged from 0.479 to 0.876 across the three species. At the population level, observed heterozygosity (H O ) ranged from 0.000 to 1.000, and expected heterozygosity (H E ) ranged from 0.091 to 0.851. In the present study, we provided the first whole-genome sequencing database for the species R. championii, identified ample SSR loci with designed primers, and revealed that 20 of the 110 selected SSRs were polymorphic across three Rhodoleia species. These provide valuable resources for future studies on genetic study, species delimitation, phylogeography, and conservation of this genus.

Hamamelidaceae (Saxifragales, previously Rosales) comprises approximately six subfamily, 30 genera and 140 species, most of which are Tertiary relicts. Exbucklandia is the only genus of the subfamily Exbucklandioideae, Hamelidaceae, containing only 2-4 species. Of them, the species E. longipetala H. T. Chang is endemic to China and listed as endangered in The Biodiversity Red List of China: Higher Plant, yet some taxonomists put forward that E. longipetala should be merged into E. tonkinensis (Lecomte) H. T. Chang. Currently, there was nearly no phylogeographic studies on this genus possibly due to the deficiency of efficient molecular markers. In this study, we sequenced the genome of E. tonkinensis based on high throughput sequencing technology, and obtained approximately 6 G raw data, which was further de novo assembled into 303,481 contigs. Based on them, 15,326 SSRs were identified from 13,596 contigs, and primers were successfully designed for 10,660 SSRs. A total of 139 paired primers were synthesized, 106 of them were successfully amplified in six Exbucklandia individuals with expected PCR product size, and 24 demonstrated to be polymorphic among three Exbucklandia populations. Accordingly, the expected and observed heterozygosity were between 0.097-0.717 and 0.098-0.583. Based on these efforts, future researches on genetic diversity and population structure of Exbucklandia can be performed to understand its phylogenetic origins and phylogeographic pattern.

Background: Pulmonary inflammation is believed to be central to the pathogenesis due to exposure to fine particulate matter with aerodynamic diameter [Formula: see text] ([Formula: see text]). This central role, however, has not yet been systemically examined., Objective: In the present study, we exploited a lung epithelial cell-specific inhibitor [Formula: see text] kinase 2 (IKK2) knockout mouse model to determine the role of pulmonary inflammation in the pathophysiology due to exposure to diesel exhaust particulate matter (DEP)., Methods: [Formula: see text] (lung epithelial cell-specific IKK2 knockout, KO) and [Formula: see text] (wild-type, tgWT) mice were intratracheally instilled with either vehicle or DEP for 4 months, and their inflammatory response and glucose homeostasis were then assessed., Results: In comparison with tgWT mice, lung epithelial cell-specific IKK2-deficient mice had fewer DEP exposure-induced bronchoalveolar lavage fluid immune cells and proinflammatory cytokines as well as fewer DEP exposure-induced circulating proinflammatory cytokines. Glucose and insulin tolerance tests revealed that lung epithelial cell-specific IKK2 deficiency resulted in markedly less DEP exposure-induced insulin resistance and greater glucose tolerance. Akt phosphorylation analyses of insulin-responsive tissues showed that DEP exposure primarily targeted hepatic insulin sensitivity. Lung epithelial cell-specific IKK2-deficient mice had significantly lower hepatic insulin resistance than tgWT mice had. Furthermore, this difference in insulin resistance was accompanied by consistent differences in hepatic insulin receptor substrate 1 serine phosphorylation and inflammatory marker expression., Discussion: Our findings suggest that in a tissue-specific knockout mouse model, an IKK2-dependent pulmonary inflammatory response was essential for the development of abnormal glucose homeostasis due to exposure to DEP. https://doi.org/10.1289/EHP4591.

Environmental stressors that encounter in early-life and cause abnormal fetal and/or neonatal development may increase susceptibility to non-communicable diseases such as diabetes. Maternal exposure to ambient fine particulate matter (PM 2.5 ) is associated with various fetal abnormalities, suggesting that it may program offspring's susceptibility to diabetes. In the present study, we therefore examined whether maternal exposure to diesel exhaust PM 2.5 (DEP), one of the major sources of ambient PM 2.5 in urban areas, programs adult offspring's glucose metabolism. Female C57Bl/6J mice were intratracheally instilled with DEP or vehicle throughout a 7-wk preconceptional period, gestation, and lactation, and the glucose homeostasis of their adult male offspring was assessed. Intraperitoneal glucose tolerance test (IPGTT) revealed that the maternal exposure to DEP significantly impaired adult male offspring's glucose tolerance. Unexpectedly, it did not influence their insulin sensitivity, whereas it significantly decreased their glucose-induced insulin secretion (GIIS). This deficit in insulin secretion was corroborated by their significant decrease in arginine-induced insulin secretion. Histological analysis demonstrated that the deficit in insulin secretion was accompanied by the decrease in pancreatic islet and β cell sizes. To differentiate the effects of maternal exposure to DEP before birth and during lactation, some offspring were cross-fostered once born. We did not observe any significant effect of cross-fostering on the glucose homeostasis of adult male offspring and the function and morphology of their β cells. Prenatal exposure to DEP programs the morphology and function of β cells and thus homeostatic regulation of glucose metabolism in adult male offspring.

Epidemiological studies link ambient fine particulate matter (PM2.5) pollution to abnormalities in the male reproductive system. However, few toxicological studies have investigated this potentially important adverse effect of PM2.5 pollution. Therefore, in the present study, we analyzed the effects of PM2.5 exposure on spermatogenesis and hypothalamic-pituitary-gonadal (HPG) axis in a murine model. Fourteen male C57BL/6J mice were subjected to a 4-month exposure to filtered air or concentrated ambient PM2.5 (CAP). Their sperm count, testicular histology, spermatogenic parameters, and the major components of HPG axis were assessed. Exposure to CAP significantly reduced sperm count in the epididymis. This was accompanied by Sertoli cell vacuolization, immature germ cell dislocation, and decreases in pachytene spermatocytes and round spermatids of stage VII seminiferous tubules, suggesting a marked impairment of spermatogenesis in these mice. This impairment of spermatogenesis appeared to be attributable to a suppression of HPG axis subsequent to CAP exposure-induced hypothalamic inflammation, as exposure to CAP significantly increased TNFα and IL1b mRNA levels and meanwhile decreased gonadotropin-releasing hormone mRNA expression in the hypothalamus. Moreover, CAP exposure significantly reduced circulating testosterone and follicle-stimulating hormone, testicular testosterone and mRNA expression of follicle-stimulating hormone target gene SHBG and luteinizing hormone target genes P450scc, 17βHSD, and StAR. The present data demonstrate that exposure to ambient PM2.5 impairs spermatogenesis in murine model, raising the concern over effects of ambient PM2.5 pollution on the male reproductive function.

The lung is constantly exposed to ambient pollutants such as ambient fine particulate matter (PM2.5), making it one of the most frequent locations of inflammation in the body. Given the establishment of crucial role of inflammation in the pathogenesis of cardiometabolic diseases, pulmonary inflammation is thus widely believed to be an important risk factor for cardiometabolic diseases. However, the causality between them has not yet been well established. To determine if pulmonary inflammation is sufficient to cause adverse cardiometabolic effects, SFTPC-rtTA+/-tetO-cre+/-pROSA-inhibitor κB kinase 2(IKK2)ca+/- (LungIKK2ca) and littermate SFTPC-rtTA+/-tetO-cre-/-pROSA-IKK2ca+/- wildtype (WT) mice were fed with doxycycline diet to induce constitutively active Ikk2 (Ikk2ca) overexpression in the lung and their pulmonary, systemic, adipose, and hypothalamic inflammations, vascular function, and glucose homeostasis were assessed. Feeding with doxycycline diet resulted in IKK2ca overexpression in the lungs of LungIKK2ca but not WT mice. This induction of IKK2ca was accompanied by marked pulmonary inflammation as evidenced by significant increases in bronchoalveolar lavage fluid leukocytes, pulmonary macrophage infiltration, and pulmonary mRNA expression of tumor necrosis factor α (Tnfα) and interleukin-6 (Il-6). This pulmonary inflammation due to lung-specific overexpression of IKK2ca was sufficient to increase circulating TNFα and IL-6 levels, adipose expression of Tnfα and Il-6 mRNA, aortic endothelial dysfunction, and systemic insulin resistance. Unexpectedly, no significant alteration in hypothalamic expression of Tnfα and Il-6 mRNA and glucose intolerance were observed in these mice. Pulmonary inflammation is sufficient to induce systemic inflammation, endothelial dysfunction, and insulin resistance, but not hypothalamic inflammation and glucose intolerance., (© The Author 2017. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.)

A series of nanofibrous alumina materials with diameters of 4-6 nm and with different aspect ratios ranging from 3 to 16 were prepared. Cobalt impregnated catalysts were prepared by means of incipient wetness impregnation on alumina nanofibers while the 'rearranged' catalysts were prepared by using ultrasonication assistance to mix the fibers with the Co 3 O 4 nanoparticles. The effects of the alumina nanofiber aspect ratios on the Co catalyst structure and performance for Fischer-Tropsch synthesis were studied. The pore size of the two series of catalysts increased as the aspect ratio of the alumina nanofiber increased. For impregnated catalysts, large Co 3 O 4 particles were formed on the external surface of the alumina support when the aspect ratio was 3 and 5, while the crystallite sizes of Co 3 O 4 increased from 13.3 nm to 15.6 nm with the increase of the aspect ratio from 7 to 16. The four 'rearranged' catalysts possessed similar and homogeneously dispersed Co 3 O 4 crystallites of 9.5 nm. As expected the reduction behavior of the two series of catalysts was primarily influenced by the Co 3 O 4 crystallite size and structure. The FT data of the two series of catalysts indicate that dispersed Co catalysts on alumina nanofibers with large aspect ratios having large inter-crystallite pores significantly improve the catalyst activity and C 5+ selectivity. The FT data of the 'rearranged' catalysts strongly demonstrated that the internal mass transfer of reactants and products increased with a decrease in inter-crystallite pore size, resulting in a decrease of C 5+ selectivity and C 3 olefin/paraffin ratio, and an increase of CH 4 selectively, while the CO consumption rate was little altered. Furthermore, catalytic stability tests showed that the alumina nanofibers with larger aspect ratios inhibited Co migration and coalescence in the matrices of the nanofibrous alumina, and this significantly enhanced the stability of the catalyst. The Co p /Al 2 O 3 -16 catalyst possessing uniformly distributed cobalt, improved reducibility and large pores is the preferred choice to generate high catalytic activity, stability and C 5+ selectivity.

This article presents a facile method to prepare CdS/SiO(2) composite microspheres and their good catalytic properties. In our method, monodispersed SiO(2) particles bearing amino groups (-NH(2)) were synthesized at first and then used as carriers to load nanosized CdS particles to form CdS/SiO(2) composite microspheres. With the addition of CdAc(2) solution to the SiO(2) dispersion, Cd(2+) was attracted to the surfaces of the SiO(2) particles through coordination interaction, and then thioacetamide was added to the dispersion. By heating, S(2-) released and reacted with the Cd(2+), CdS/SiO(2) composite microspheres were obtained accordingly. The photocatalytic properties of the as-prepared composite microspheres were investigated as well. It was found that the composite microspheres have excellent photocatalytic activities for the degradation of dyes comparing with the commercial P-25 TiO(2) catalysts. After using and recycling for three times, the photocatalytic performance still remained very well., (© 2012 Wiley Periodicals, Inc. Photochemistry and Photobiology © 2012 The American Society of Photobiology.)

Increasing evidence suggests that celecoxib, a COX-2 inhibitor with potent anticancer activity exerts its effects not only through COX-2, but also through COX-2-independent mechanisms. In the present study, we hypothesized that endoplasmic reticulum stress (ERS) is involved in the up-regulation of VEGF expression induced by celecoxib in colorectal cancer HCT116 cells and that ERS is a major mechanism by which celecoxib triggers tumor cell death in a COX-2-independent manner. HCT116 cells, which do not express COX-2, were cultured in the absence or presence of celecoxib. VEGF expression was detected by quantitative real-time RT-PCR and western blotting. ERS triggered by celecoxib was determined by expression of ER chaperones and other markers. PBA (an inhibitor of ERS) and GRP78 overexpression were both used to prevent ERS. Cell apoptosis was evaluated by TUNEL assay and fluorescence activated cell sorting. In HCT116 cells, celecoxib increased VEGF production with time-course and dose-response curves similar to those observed for the increase of the ER chaperone, GRP78. CHOP, a marker of ERS involved in apoptosis, was also increased by celecoxib. Moreover, celecoxib promoted cell apoptosis. Both apoptosis and up-regulation of VEGF were prevented by protecting cells from ERS. Celecoxib induces cell apoptosis and up-regulation of VEGF in HCT116 cells via activation of the ERS response. Further studies are necessary to evaluate whether the combination of celecoxib with anti-VEGF agents is a promising therapeutic modality for cancer.