Aligned films of a semiconducting DPP‐based copolymer exhibit highly anisotropic charge transport with a band‐like temperature dependence along the alignment direction and hole mobilities of up to 6.7 cm2 V−1 s−1. X‐ray diffraction measurements reveal an exceptional degree of in‐plane alignment, high crystallinity, and a dominant face‐on orientation of the polymer backbones. The surprising charge‐transport properties are interpreted in a tie‐chain model consistent with anisotropic activation energies.

Tumor-associated macrophages are associated with poor prognosis in certain cancers. Monocyte chemoattractant protein 1 (MCP-1) is thought to be the most important chemokine for recruitment of macrophages to the tumor microenvironment. However, its role on tumorigenesis in a genetic mouse model of colon cancer has not been explored. We examined the role of MCP-1 on tumor-associated macrophages, inflammation, and intestinal tumorigenesis. Male Apc Min/+, Apc Min/+/MCP-1−/− or wild-type mice were euthanized at 18 wk of age and intestines were analyzed for polyp burden, apoptosis, proliferation, β-catenin, macrophage number and phenotype, markers for cytotoxic T lymphocytes and regulatory T cells, and inflammatory mediators. MCP-1 deficiency decreased overall polyp number by 20% and specifically large polyp number by 45% ( P < 0.05). This was consistent with an increase in apoptotic cells ( P < 0.05), but there was no change detected in proliferation or β-catenin. MCP-1 deficiency decreased F4/80-positive cells in both the polyp tissue and surrounding intestinal tissue ( P < 0.05) as well as expression of markers associated with M1 (IL-12 and IL-23) and M2 macrophages (IL-13, CD206, TGF-β, and CCL17) ( P < 0.05). MCP-1 knockout was also associated with increased cytotoxic T lymphocytes and decreased regulatory T cells ( P < 0.05). In addition, MCP-1−/− offset the increased mRNA expression of IL-1β and IL-6 in intestinal tissue and IL-1β and TNF-α in polyp tissue ( P < 0.05), and prevented the decrease in SOCS1 expression ( P < 0.05). We demonstrate that MCP-1 is an important mediator of tumor growth and immune regulation that may serve as an important biomarker and/or therapeutic target in colon cancer.

No abstract

In this article we discuss the synthesis of four new low band-gap co-polymers based on the diketopyrrolopyrrole (DPP) and benzotriazole (BTZ) monomer unit.

Evidence suggests that serum brain-derived neurotrophic factor (serum BDNF) can be affected by cardiorespiratory fitness (CRF), but this relationship is far from clear. Recent reports show an inverse relationship between serum BDNF and CRF in healthy individuals, and other studies suggest a possible association between serum BDNF and cardiovascular disease. However, the possible interaction between serum BDNF, CRF, and cardiovascular disease risk has not been studied. The purpose of this study was to examine the association among serum BDNF, CRF, and cardiovascular disease risk factors in healthy men. The investigation involved a large sample of men (n = 995, age range: 20-76 years) who live in the central area of South Korea and were recruited into the Preventive Health Study. Our study showed a significant inverse relationship between serum BDNF and relative VO(2)max (r = -0.412, p < 0.0001) and heart rate reserve (r = -0.194, p < 0.0001). Serum BDNF was positively correlated with body mass index (r = 0.80, p < 0.0001), total cholesterol (r = 0.185, p < 0.0001), and triglyceride (r = 0.320, p < 0.0001). Our data suggest that serum BDNF may be associated with effects of increased CRF on cardiovascular disease. However, more research is clearly needed before a determination of whether, and to what extent, serum BDNF may be responsible for some of the health benefits associated with CRF.

Increased free radical production and oxidative damage in ageing muscle may be a contributing factor to the development of sarcopenia. It has been suggested that the accumulation of iron may be an underlying factor in the development of oxidative stress in ageing tissues, including skeletal muscle. At present, however, the mechanisms responsible for ageing-associated muscle iron accumulation are unknown. These experiments tested the hypothesis that ageing-associated elevations in skeletal muscle iron are accompanied by altered expression of key regulators of intracellular iron status. We determined non-haem iron, oxidative injury, and expression levels of iron regulation proteins in plantaris muscles harvested from 6-and 24-to 26-month-old Fisher 344 rats (n = 10 per group). Ageing resulted in a 62% elevation in skeletal muscle nonhaem iron (P < 0.05) and higher protein oxidative damage (P < 0.05). Notably, ageing was associated with elevated expression of ferritin (heavy chain, +56.2-fold; light chain, +7.3-fold), an important iron storage protein. Conversely, the iron transport protein transferrin receptor-1 demonstrated dramatic downregulation (−10.8-fold; P < 0.05) in old muscle, whereas the level of divalent metal transporter-1 protein expression was unaltered. No change in protein level of iron regulatory protein-1 was observed. In summary, these results demonstrate the occurrence of altered iron regulation concomitant with iron accumulation and oxidative stress in aged skeletal muscle. Importantly, the maintenance of divalent metal transporter-1 protein expression into old age could play a role in the accumulation of skeletal muscle iron.

A ready-made, acellular patch-type prosthesis is desirable in repairing partial tracheal defects in the clinical setting. However, many of these prostheses may not show proper biological integration and biomechanical function when they are transplanted. In this study, we developed a novel 3D printed polyurethane (PU) tracheal scaffold with micro-scale architecture to allow host tissue infiltration and adequate biomechanical properties to withstand physiological tracheal condition. A half-pipe shaped PU scaffold (1.8 cm of height, 0.18 cm thickness, and 2 cm of diameter) was fabricated by 3D printing of PU 200 μm PU beam. The 3D printed tracheal scaffolds consisted of a porous inner microstructure with 200 × 200 × 200 μm sized pores and a non-porous outer layer. The mechanical properties of the scaffolds were 3.21 ± 1.02 MPa of ultimate tensile strength, 2.81 ± 0.58 MPa of Young's modulus, and 725% ± 41% of elongation at break. To examine the function of the 3D printed tracheal scaffolds in vivo, the scaffolds were implanted into 1.0 × 0.7 cm sized anterior tracheal defect of rabbits. After implantation, bronchoscopic examinations revealed that the implanted tracheal scaffolds were patent for a 16 week-period. Histologic findings showed that re-epithelialization after 4 weeks of implantation and ciliated respiratory epithelium with ciliary beating after 8 weeks of implantation were observed at the lumen of the implanted tracheal scaffolds. The ingrowth of the connective tissue into the scaffolds was observed at 4 weeks after implantation. The biomechanical properties of the implanted tracheal scaffolds were continually maintained for 16 week-period. The results demonstrated that 3D printed tracheal scaffold could provide an alternative solution as a therapeutic treatment for partial tracheal defects.

Nutritional ketosis may enhance cerebral energy metabolism and has received increased interest as a way to improve or preserve performance and resilience. Most studies to date have focused on metabolic or neurological disorders while anecdotal evidence suggests that ketosis may enhance performance in the absence of underlying dysfunction. Moreover, decreased availability of glucose in the brain following stressful events is associated with impaired cognition, suggesting the need for more efficient energy sources. We tested the hypotheses that ketosis induced by endogenous or exogenous ketones could: (a) augment cognitive outcomes in healthy subjects; and (b) prevent stress-induced detriments in cognitive parameters. Adult, male, Sprague Dawley rats were used to investigate metabolic and behavioral outcomes in 3 dietary conditions: ketogenic (KD), ketone supplemented (KS), or NIH-31 control diet in both control or chronic stress conditions. Acute administration of exogenous ketones resulted in reduction in blood glucose and sustained ketosis. Chronic experiments showed that in control conditions, only KD resulted in pronounced metabolic alterations and improved performance in the novel object recognition test. The hypothalamic-pituitary-adrenal (HPA) axis response revealed that KD-fed rats maintained peripheral ketosis despite increases in glucose whereas no diet effects were observed in ACTH or CORT levels. Both KD and KS-fed rats decreased escape latencies on the third day of water maze, whereas only KD prevented stress-induced deficits on the last testing day and improved probe test performance. Stress-induced decrease in hippocampal levels of β-hydroxybutyrate was attenuated in KD group while both KD and KS prevented stress effects on BDNF levels. Mitochondrial enzymes associated with ketogenesis were increased in both KD and KS hippocampal samples and both endothelial and neuronal glucose transporters were affected by stress but only in the control diet group. Our results highlight the complex relationship between peripheral metabolism, behavioral performance and biochemical changes in the hippocampus. Endogenous ketosis improved behavioral and metabolic parameters associated with energy metabolism and cognition while ketone supplementation replicated the biochemical effects within the hippocampus but only showed modest effects on behavioral improvements.