4,4′-Bipyrid­yl–4,4′-(hy­droxy­methyl­ene)dibenzoic acid (1/1)

In the title 1:1 co-crystal, C10H8N2·C15H12O5, strong inter­molecular O—H⋯N hydrogen bonds link alternating mol­ecules of 4,4′-(hy­droxy­methyl­ene)dibenzoic acid and 4,4′-bipyridyl into zigzag chains in [501]. The crystal packing also exhibits π–π inter­actions between the 4,4′-bipyridyl rings of neighbouring chains [centroid–centroid distance = 3.608 (3) Å] and weak C—H⋯O hydrogen bonds

Bis(dimethyl­ammonium) 2,2′-(1,3,6,8-tetra­oxo-2,7-diaza­pyrene-2,7-di­yl)diacetate

The asymmetric unit of title compound, 2C2H8N+·C18H8N2O8 2−, comprises one crystallographically independent dimethyl­ammonium cation and half of a 2,2′-(1,3,6,8-tetra­oxo-2,7-diaza­pyrene-2,7-di­yl)diacetate dianion. The anion lies on an inversion centre and the two carboxyl­ate groups are in trans positions based on the naphthaleneteracarb­oxy­lic diimide group. The crystal packing is stabilized by N—H⋯O hydrogen bonds between cations and anions, as well as by π–π inter­actions between the naph­thaleneteracarb­oxy­lic diimide groups [centroid–centroid distance = 4.812 (3) Å]

Adrenaline inhibited cell proliferation and regulated expression of TGF-beta1 and bFGF in cultured human hypertrophic scar fibroblasts via alpha-receptor

Adrenaline has been shown to modulate proliferation of mouse fibroblasts, adventitial fibroblasts and synovial B (fibroblasts-like) cells. However, little is known about the response of cultured human hypertrophic scar fibroblasts to adrenaline. In this study, we investigated cell proliferation and involved mechanisms in hypertrophic scar fibroblasts in response to adrenaline. Population doubling time (PDT) assay and MTT assay were performed to determine the cell proliferation and cell viability, respectively. The expression of bFGF and TGF- ß1 was measured by reverse transcriptase-polymerase chain reaction (RT-PCR) and enzyme linked immunosorbent assay (ELISA). The results showed that adrenaline inhibited proliferation of normal and hypertrophic scar fibroblasts in a dose-dependent manner. Moreover, adrenaline up-regulated the expression of bFGF and down-regulated the expression of TGF- ß1 in normal and hypertrophic scar fibroblasts. Interestingly incubation with the a receptor antagonist regitine indicated that adrenaline mediated inhibition of cell proliferation and regulation of TGF-ß1 and bFGF in cultured normal and hypertrophic scar fibroblasts were mediated by the a receptor. These studies suggest that adrenaline inhibits proliferation and alters the expression of TGF-ß1 and bFGF in human hypertrophic scar fibroblast involving an a receptor mediated pathway

A63: Exercise Improves Appetite and Heart Function in High Fat Drosophila

Purpose: High-fat diets cause obesity and disease leading to excess appetite and cardiovascular disease. At present, there is literature showing the improvement effect of exercise on obesity and related diseases. To explore more deeply the mechanism of action of exercise on appetite improvement and heart function in high-fat diets, we used fruit fly motility models to reveal this aspect of function. Methods: A total of 300 wild-type W1118 virgin flies that matured within 12 hours were collected. They were randomly divided into 100 animals in the normal diet control group (NFD), 100 in the high-fat diet group (HFD), and 100 in the high-fat diet exercise group (HFD+E). Exercise intervention for 7-day-old fruit flies for 5 consecutive days. An EM-CCD high-speed camera was used to record the heartbeat of fruit flies (video at 130 fps, the 30 s), and HC Image software was used to record the cardiogram data. Semi-Automated Optical Heartbeat Analysis (SOHA) quantifies Heart Rate (HR), Heart Period (HP), Diastolic Intervals (DI), Systolic Intervals (SI), Arrhythmia Index (AI), Diastolic Diameter (DD), Systolic Diameter (SD), Fractional Shortening (FS), and Fibrillations (FL). Fruit fly uptake was measured using the FlyPAD high-throughput Drosophila quantitative feeding system. All fruit flies needed to be fed on normal medium for 5 days first and then transferred to fresh normal medium or the high-fat medium on the 6th day for another 2 days. NFD flies are placed in a constant temperature and humidity incubator (25 ℃, 50% humidity, 12 h day and night cycle), HFD flies are housed in incubators at 22-24 ℃ and 50% relative humidity to make high-fat medium by mixing 30% coconut oil and 70% standard medium. Results: The HFD group had an increase in AI, HR and HP, constant SD, decreased DD, and decreased FS. After exercise, HFD+E group had a decrease in HR, an increase in HP, an improvement in AI, an improvement in DD, and no change in SD. The food intake and sipping frequency of fruit flies in the HFD group were significantly higher than those in the NFD group, and during the same time period, the food intake and number of sipping times in the HFD+E group and the HFD group decreased significantly after exercise. Conclusion: Exercise improved excess appetite and cardiac dysfunction in high-fat diets

Epileptiform discharge upregulates p-ERK1/2, growth-associated protein 43 and synaptophysin in cultured rat hippocampal neurons

AbstractExtracellular signal-regulated protein kinase, ERK1/2 is activated by phosphorylation (p-ERK1/2) during environmental stress such as epileptiform discharge. We investigated the role of ERK1/2 in abnormal axon growth and synapse reorganization in cultured neurons displaying epileptiform activity.The cultured neurons displaying epileptiform activity were treated with magnesium-free extracellular fluid for 3h and monitored epileptiform discharges using whole-cell patch clamp. Two study groups, neurons displaying epileptiform activity and the same neurons treated with ERK1/2 inhibitor U0126, were studied at six time points, 0min, 30min, 2h, 6h, 12h, and 24h following discharge. The expressions of p-ERK1/2, C-fos, growth-associated protein 43 (GAP-43) and synaptophysin (SYP), as markers of axon growth and synapse reorganization, were investigated by double-label immunofluorescence and western blotting.In the neurons displaying epileptiform activity, p-ERK1/2 was detected immediately following discharge, and expression peaked at 30min. The expression of C-fos, GAP-43 and SYP followed the same pattern as p-ERK1/2. In the treated group, p-ERK1/2 was inhibited completely, and C-fos, GAP-43 and SYP were reduced.These findings indicate that epileptiform discharge activates ERK1/2 which regulates C-fos in cultured neurons displaying epileptiform activity, and this cascade may upregulate GAP-43 and SYP to contribute to axon growth and synapse reorganization to potentiate epileptic activities

SPIDER-WEB enables stable, repairable, and encryptible algorithms under arbitrary local biochemical constraints in DNA-based storage

DNA has been considered as a promising medium for storing digital information. Despite the biochemical progress in DNA synthesis and sequencing, novel coding algorithms need to be constructed under the specific constraints in DNA-based storage. Many functional operations and storage carriers were introduced in recent years, bringing in various biochemical constraints including but not confined to long single-nucleotide repeats and abnormal GC content. Existing coding algorithms are not applicable or unstable due to more local biochemical constraints and their combinations. In this paper, we design a graph-based architecture, named SPIDER-WEB, to generate corresponding graph-based algorithms under arbitrary local biochemical constraints. These generated coding algorithms could be used to encode arbitrary digital data as DNA sequences directly or served as a benchmark for the follow-up construction of coding algorithms. To further consider recovery and security issues existing in the storage field, it also provides pluggable algorithmic patches based on the generated coding algorithms: path-based correcting and mapping shuffling. They provide approaches for probabilistic error correction and symmetric encryption respectively.Comment: 30 pages; 12 figures; 2 table