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Bird feathers have aroused tremendous attention for their superdurability against tears during long flights through wind and even bushes. Although feathers may inevitably be unzipped, the separated feather vanes can be repaired easily by bill stroking. However, the mechanism underlying bird feathers' superdurability against tears remains unclear. Here, we reveal that the superdurability of bird feathers arises from their repairable cascaded slidelock system, which is composed of hooklets, a slide rail, and spines at the end of the slide rail as terminating structures. Microscopy with a micronano manipulating system and 3D X-ray microscopy provided high-level visibility into the 3D fine structures and the entire unzipping process of feathers. The hooklets can slide along the slide rail reversibly when suffering external forces, and the sliding hooklet can be locked by the spine at the ends of barbules when larger pulling forces are applied and even slide farther away due to the unzipping of the interlocking structure with large deformation of the barbules. The elongation before separation of adjacent barbs can reach up to 270%, and the separation force can be maintained above 80% of the initial value even after 1,000 cycles of separating and repairing. These results prove that the cascaded slide-lock system ensures the superdurability of bird feathers against tears. [ABSTRACT FROM AUTHOR]

A hierarchical assembled ITO nanowire array with both horizontal and vertical nanowire branches was fabricated as a new three-dimensional fractal nanobiointerface for efficient cancer cell capture. Comparing with ITO nanowire array without branches, this fractal nanobiointerface exhibited much higher efficiency (89% vs 67%) and specificity in capturing cancer cells and took shorter time (35 vs 45 min) to reach the maximal capture efficiency. As indicated by the immunofluorescent and ESEM images, this enhancement can be attributed to the improvement of topographical interaction between cells and the substrate. The introduction of horizontal and vertical nanowire branches makes the substrate topographically match better with cell filopodia and provides more binding sites for cell capture. The live/dead cell staining and proliferation experiments confirm that this fractal nanobiointerface displays excellent cyto-compatibility with an over 96% cell viability after capture. These results provide new insights and may open up opportunities in designing and engineering new cell-material interfaces for advanced biomedical applications. [ABSTRACT FROM AUTHOR]

The tetratricopeptide repeat (TPR)-containing protein FLU is a negative regulator of chlorophyll biosynthesis in plants. It directly interacts through its TPR domain with glutamyl-tRNA reductase (GluTR), the rate-limiting enzyme in the formation of δ-aminolevulinic acid (ALA). Delineation of how FLU binds to GluTR is important for understanding the molecular basis for FLU-mediated repression of synthesis of ALA, the universal tetrapyrrole precursor. Here, we characterize the FLU-GluTR interaction by solving the crystal structures of the uncomplexed TPR domain of FLU (FLUTPR) at 1.45-Å resolution and the complex of the dimeric domain of GluTR bound to FLUTPR at 2.4-Å resolution. Three non-canonical TPR motifs of each FLUTPR form a concave surface and clamp the helix bundle in the C-terminal dimeric domain of GluTR. We demonstrate that a 2:2 FLUTPR-GluTR complex is the functional unit for FLU-mediated GluTR regulation and suggest that the formation of the FLU-GluTR complex prevents glutamyl-tRNA, the GluTR substrate, from binding with this enzyme. These results also provide insights into the spatial regulation of ALA synthesis by the membrane-located FLU protein. [ABSTRACT FROM AUTHOR]

Background: This study aimed to analyze the factors influencing warfarin-related major gastrointestinal bleeding (GIB) and to develop a score that would provide a reference for assessing the risk of major GIB associated with warfarin treatment. Methods: This was a retrospective analysis of clinical and follow-up data from warfarin-treated patients. Scores were analyzed using logistic regression. The area under the subject working characteristic curve (AUC), sensitivity, specificity, and Hosmer-Lemeshow test were used to evaluate the scoring performance. Results: A total of 1591 patients who met the requirements for warfarin use were included in this study, and 46 developed major GIB. After univariate analysis as well as multivariate logistic regression analysis, nine factors were found to be associated with increased risk of major GIB, namely age ≥ 65 years, history of peptic ulcer, history of major bleeding, abnormal liver function, abnormal renal function, cancer, anemia, labile international normalized ratio, and combination of antiplatelet agents/non-steroidal anti-inflammatory drugs. The Alfalfa-Warfarin-GIB score was constructed using these nine factors. The AUC and Bootstrap method-corrected AUC of the Alfalfa-Warfarin-GIB score were 0.916 (95% CI: 0.862–0.970, P < 0.001) and 0.919 (95% CI: 0.860–0.967, P < 0.001), respectively, which were higher than those of the HAS-BLED score (AUC = 0.868, 95% CI: 0.812–0.924, P < 0.001). Conclusion: Based on nine risk factors, the Alfalfa-Warfarin-GIB score was constructed to predict the risk of warfarin-related major GIB. The newly developed Alfalfa-Warfarin-GIB score has a better predictive value than the HAS-BLED score and may be an effective tool to help reduce the occurrence of major GIB in patients on warfarin. [ABSTRACT FROM AUTHOR]

The article informs that according to a study exercise training improves motor skill learning through selective activation of mechanistic target of rapamycin (mTOR.) It mentions that mTOR activation leads to potentiated postsynaptic excitation and enhanced neuronal activity of pyramidal neurons after exercise, with increased oligodendrogenesis and axonal myelination. It informs that neural network through exercise supports the intervention of cognitive deficits using exercise training.

Underwater superoleophobic surfaces have attracted great attention due to their broad applications such as anti-oil adhesion, oil capture and transportation, and oil/water separation. However, it is often fairly complex and time-consuming, involved in the construction of micro/nanostructures and the regulation of chemical compositions; there is an urgent need to develop new strategies to conquer these problems. Inspired by the strong anchoring capability and easy accessibility of plant polyphenols, we can readily and rapidly fabricate tannic acid (TA) coated copper surfaces with the excellent underwater super oil-repellent property. To achieve the optimal condition for TA modification, the influence of immersion time, TA concentration, and pH value on underwater-oil wettability and adhesion has been systematically explored. Furthermore, the underwater super oil-repellent feature can be widely achieved for different oils and on various metal sheets, suggesting the potential applications for plenty of fields such as anti-oil pollution. [ABSTRACT FROM AUTHOR]

Resveratrol could be beneficial to health and provides protection against a wide array of pathologies and age-associated problems, as evident from preclinical studies. However, a comparison of animal and human studies reveals that this dietary polyphenol cannot protect against metabolic diseases and their associated complications. The clinical outcomes are affected by many factors such as sample size. This article not only presents a comprehensive review of the current advances concerning the dose, the extent of absorption, interaction and toxicity of resveratrol in human studies, but also describes its therapeutic effects against several chronic diseases such as diabetes mellitus, obesity, cardiovascular diseases, cancer and aging and the related diseases. [ABSTRACT FROM AUTHOR]

Background: The nematode Caenorhabditis elegans is both sensitive and tolerant to hypoxic stress, particularly when the evolutionarily conserved hypoxia response pathway HIF-1/EGL-9/VHL is involved. Hypoxia-induced changes in the expression of a number of genes have been analyzed using whole genome microarrays in C. elegans, but the changes at the protein level in response to hypoxic stress still remain unclear. Results: Here, we utilized a quantitative proteomic approach to evaluate changes in the expression patterns of proteins during the early response to hypoxia in C. elegans. Two-dimensional difference gel electrophoresis (2D-DIGE) was used to compare the proteomic maps of wild type C. elegans strain N2 under a 4-h hypoxia treatment (0.2% oxygen) and under normoxia (control). A subsequent analysis by MALDI-TOF-TOF-MS revealed nineteen protein spots that were differentially expressed. Nine of the protein spots were significantly upregulated, and ten were downregulated upon hypoxic stress. Three of the upregulated proteins were involved in cytoskeletal function (LEV-11, MLC-1, ACT-4), while another three upregulated (ATP-2, ATP-5, VHA-8) were ATP synthases functionally related to energy metabolism. Four ribosomal proteins (RPL-7, RPL-8, RPL-21, RPS-8) were downregulated, indicating a decrease in the level of protein translation upon hypoxic stress. The overexpression of tropomyosin (LEV-11) was further validated by Western blot. In addition, the mutant strain of lev-11(x12) also showed a hypoxia-sensitive phenotype in subsequent analyses, confirming the proteomic findings. Conclusions: Taken together, our data suggest that altered protein expression, structural protein remodeling, and the reduction of translation might play important roles in the early response to oxygen deprivation in C. elegans, and this information will help broaden our knowledge on the mechanism of hypoxia response. [ABSTRACT FROM AUTHOR]

The objective of this study was to evaluate the effects of specific NF-κB inhibitor pyrrolidine dithiocarbamate (PDTC) on inflammatory response and cardiac function in a rat model of coronary microembolization (CME). CME was developed by injecting a suspension of microthrombotic particles (MTPs) into the left ventricle when obstructing the ascending aorta. MTPs were generated from the rat clots sized by filtration through 38 μm screen. Thirty-two Sprague–Dawley rats served as sham group, 128 CME rats were randomized to untreated (CMEU) and PDTC-treated (CMEp) group. Rats in CMEp were administered intraperitoneally with 50, 100, 200 mg kg−1 day−1 PDTC, respectively, from 1 h before to 7 days after operation. The rats were sacrificed on day 1, 3, 7, 14 post-operationally and each subgroup consisted of eight rats. The general morphological characteristics were observed in sections with HE staining, and the severity of myocardial loss (SML) was determined by percent micro-necrotic area in sections with hematoxylin basic fuchsin picric (HBFP) staining 1 day or by percent micro-fibrotic area in sections with Masson’s trichrome staining 14 days post-operationally. Left ventricular (LV) function was evaluated echocardiographically and hemodynamically. Activity of NF-κB/DNA-binding was analyzed by electrophoresis mobility shift assays (EMSA), and expressions of TNF-α, IL-6, and ICAM-1 genes and proteins were detected by Real-time PCR and western blots, respectively. CME rats exhibited pathological changes evidenced by multi-focal myocardial necrosis, inflammatory cell infiltration with remarkably increased SML and persistent reduction of LV function. Activity of NF-κB/DNA-binding was markedly increased, also TNF-α, IL-6 and ICAM-1 transcripts and their protein expressions were upregulated strongly in the myocardium following CME. PDTC in a dose-dependency significantly suppressed the myocardial inflammatory cytokine transcriptions, decreased SML and improved LV function. Thus, NF-κB is markedly activated in CME hearts, and inhibition of NF-κB by PDTC prevents the subsequent inflammatory activation and improves cardiac function. Patients with or at risk of CME may benefit from acute anti-inflammatory treatment with PDTC. [ABSTRACT FROM AUTHOR]