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Morphine is a potent agonist of μ-opioid receptor and is widely used to relieve severe pain, including cancer pain. Some chemokines, for example, CX3CL1 and CCL2, participate in the regulation of opioid santinociception. In our previous study, we found overexpression of chemokine CXCL10/CXCR3 in spinal cord participated in the development of cancer-induced bone pain, so we supposed that CXCL10 may have influence in morphine analgesia in cancer pain relief. In this study, we found that a single dose of morphine could transiently increase the expression of CXCL10 in spinal cord. Blocking the function of CXCL10 enhanced morphine antinociception in cancer-induced bone pain rats. However, overexpression of CXCL10 induced acute algesia and decreased the analgesic effect of morphine in normal mice. The algesic effect of CXCL10 was blocked by inhibition of CXCR3 and Gi protein. These results suggested that CXCL10 in spinal cord serves as a novel negative regulator of morphine analgesia and provided evidence that activation of CXCL10/CXCR3 in spinal cord may attenuate antinociceptive potency of morphine in cancer pain relief.

CX3CL1 (fractalkine), the sole member of chemokine CX3C family, is implicated in inflammatory and neuropathic pain via activating its receptor CX3CR1 on neural cells in spinal cord. However, it has not been fully elucidated whether CX3CL1 or CX3CR1 contributes to the development of morphine tolerance. In this study, we found that chronic morphine exposure did not alter the expressions of CX3CL1 and CX3CR1 in spinal cord. And neither exogenous CX3CL1 nor CX3CR1 inhibitor could affect the development of morphine tolerance. The cellular localizations of spinal CX3CL1 and CX3CR1 changed from neuron and microglia, respectively, to all the neural cells during the development of morphine tolerance. A microarray profiling revealed that 15 members of chemokine family excluding CX3CL1 and CX3CR1 were up-regulated in morphine-treated rats. Our study provides evidence that spinal CX3CL1 and CX3CR1 may not be involved in the development of morphine tolerance directly.

Asian seabass (Lates calcarifer ) is becoming an important species for aquaculture. However, the Asian seabass aquaculture industry faces a significant challenge of disease outbreaks that can jeopardize fish health and production. This review delves into the major diseases affecting Asian seabass aquaculture and explores their causes, symptoms, and management approaches. We focused on the key pathogens responsible for these outbreaks, the environmental factors contributing to disease susceptibility, and the latest advancements in disease prevention and management. By addressing these critical aspects, this review addresses the needs of aquaculturists, researchers, and policymakers with the knowledge required to promote resilient and sustainable Asian seabass farming. We aim to shed light on the challenges posed by disease while highlighting innovative strategies that offer promise for the future of this thriving industry. This comprehensive examination serves as a valuable resource for those invested in ensuring the health and vitality of Asian seabass, securing a consistent supply to meet the demands of global seafood markets.

A greenhouse study was conducted to evaluate the growth and development of poinsettia ‘Prestige Red’ (Euphorbia pulcherrima) grown in a commercial peat-based potting mix (Sunshine Mix #1) amended with biochar at 0%, 20%, 40%, 60%, 80%, or 100% (by volume) at four different fertigation regimes: F1: 100 to 200 mg·L−1 nitrogen (N), F2: 200 to 300 mg·L−1 N (control), F3: 300 to 400 mg·L−1 N, or F4: 400 to 500 mg·L−1 N. The experiment was a two-factor factorial design with 10 replications for each combination of biochar by fertigation. As the percentage of biochar increased, root substrate pore space and bulk density increased, while container capacity decreased. Root rot and red bract necrosis only occurred in F4 combined with 100% biochar. Plants grown in 40% biochar had a similar growth and development to those in 0% biochar. Up to 80% biochar, plants exhibited no significant change, except in terms of dry weight, which decreased at higher biochar percentages (60% and 80%). In summary, at a fertigation rate of 100 mg·L−1 N to 400 mg·L−1 N, up to 80% biochar could be used as an amendment to peat-based root substrate with acceptable growth reduction and no changes in quality.

A simple approach for preparing recycled poly(ethylene terephthalate) (r-PET) with excellent processability and melt strength has been developed in this research. To increase the intrinsic viscosity of r-PET, a two-step chain extension process using a combination of SAG-008 and tetraglycidyl-4,4′-diaminodiphenylmethane (TGDDM) was investigated. To evaluate the chain extension degree of the modified r-PET, its intrinsic viscosity (IV) and rheological properties were characterized, and found to be correlated to the long-chain branches and molecular weight. The results indicated that the combination of SAG-008 and TGDDM at the optimized conditions provided the highest IV of 1.18 dl/g while controlling the gel formation to a low value. The increases in storage modulus, loss modulus and complex viscosity revealed the enhancement of melt strength and viscoelasticity of r-PET. The differential scanning calorimetry results showed that the crystallinity was reduced with the addition of chain extenders. On the other hand, stepwise annealing method from room temperature to crystal melting temperature promoted the crystallization, which was confirmed by wide-angle X-ray diffraction measurement.

Cell-cell coupling via gap junctions has been extensively studied in vitro and in heterologous systems, but in vivo studies are still few. A new class of photoactivatable bioconjugates is now used to monitor gap junctional coupling in living Caenorhabditis elegans . To study the physiological regulation and function of cell-cell gap junction communication in vivo , we developed a bioconjugate of caged dye, named dextran-CANPE-HCC, for imaging cell coupling in small model organisms. In vitro , the compound was photolyzed efficiently with robust fluorescence enhancement. Dextran-CANPE-HCC delivered into Caenorhabditis elegans oocytes was retained in cells throughout development. Using local uncaging, we photolyzed dextran-CANPE-HCC to release the small HCC dye and imaged the dynamics of intercellular dye transfer through gap junction channels, a technique we named Trojan–local activation of molecular fluorescent probes (LAMP). Early during embryonic development, the pattern of cell coupling undergoes dramatic remodeling and imaging revealed that the germ cell precursors, P2, P3 and P4, were isolated from the somatic cell communication compartment. As dextran-CANPE-HCC is chemically and metabolically stable, labeled worms showed very bright signal upon photoactivation after hatching, which allowed us to examine cell coupling in living worms noninvasively.

The aim of the present study was to analyze the effect of temozolomide (TMZ) on the antiapoptotic gene livin and the associated gene caspase-3. Cancer stem cells were isolated from U251 glioblastoma cells using immunomagnetic beads. The glioma cells and glioma stem cells were transfected with livin or small hairpin RNA (shRNA) against livin using lentiviral vectors. Quantitative PCR, flow cytometry and a Cell Counting kit-8 assay were used to detect the expression of livin and caspase-3, analyze the cell cycle and investigate cell proliferation, respectively, following treatment with various concentrations of TMZ (0, 25, 50, 100, 200 and 400 μmol/l) for different periods of time (24, 48 and 72 h). The expression levels of livin and caspase-3 in the U251 stem cells were significantly higher than those in the U251 cells (P<0.01). At the same intervention time, the expression levels of livin decreased and those of caspase-3 increased as the concentration of TMZ increased (P<0.05). The expression levels of livin and caspase-3 in the U251 cells were lower than those in the U251 stem cells with the same intervention time and concentration of TMZ (P<0.05). The cell cycle was arrested in the G2/M phase in the U251 cells following TMZ intervention; the proportion of cells in the G2/M phase increased as the concentration of TMZ increased (P<0.05). The U251 stem cells were arrested in the S phase following treatment with TMZ; the proportion of cells in the S phase increased as the concentration of TMZ increased (P<0.05). In conclusion, the expression levels of livin and caspase-3 were effectively inhibited and increased, respectively, in all cell models following treatment with TMZ. TMZ is able to arrest the cell cycle and enhance cell apoptosis. U251 stem cells are less vulnerable than U251 cells to TMZ.