Global warming is one of the most common environmental challenges faced by cold-water fish farming. Heat stress seriously affects the feeding, growth, immunity, and disease resistance of fish. These changes are closely related to the destruction of intestinal barrier function, the change of intestinal microbiota, and metabolic dysfunction.
View Article and Find Full Text PDFAs the global climate warms, more creatures are threatened by high temperatures, especially cold-water fish such as rainbow trout. Evidence has demonstrated that long noncoding RNAs (lncRNAs) play a pivotal role in regulating heat stress in animals, but we have little understanding of this regulatory mechanism. The present study aimed to identify potential key lncRNAs involved in regulating acute heat stress in rainbow trout.
View Article and Find Full Text PDFHeat stress is a condition in which the body's homeostasis is disturbed as a result of the rise in water temperature, resulting in the decline or even death of growth, immunity, and other functions. The mechanisms directing this response are not fully understood. To better characterize the effects of acute heat stress on the innate immune function of rainbow trout, we identified differentially regulated messenger RNA (mRNA) and non-coding RNA (ncRNA) in rainbow trout exposed to acute heat stress.
View Article and Find Full Text PDFWe have developed a novel wet extrusion process to fabricate nonwoven self-assembled microfiber scaffolds with uniform diameters less than 5 μm and without any postmanipulation. In this method, a poly(L-lactic acid) solution flows dropwise into a stirring nonsolvent bath, deforming into liquid polymer streams that self-assemble into a nonwoven microfiber scaffold. The ability to tune fiber diameter was achieved by decreasing polymer spin dope concentration and increasing the silicon oil to petroleum ether ratio of the nonsolvent spin bath.
View Article and Find Full Text PDFThe maturation of cardiac myocytes during the immediate prenatal period coincides with changes in the mechanical properties of the extracellular matrix. We investigated the effects of extracellular stiffness on cardiomyocyte maturation in neonatal rat ventricular myocytes grown on collagen-coated gels. Cells on 10-kPa substrates developed aligned sarcomeres, while cells on stiffer substrates had unaligned sarcomeres and stress fibers.
View Article and Find Full Text PDFVarious types of cardiomyocytes undergo changes in automaticity and electrical properties during fetal heart development. Human embryonic stem cell-derived cardiomyocytes (hESC-CMs), like fetal cardiomyocytes, are electrophysiologically immature and exhibit automaticity. We used hESC-CMs to investigate developmental changes in mechanisms of automaticity and to determine whether electrophysiological maturation is driven by an intrinsic developmental clock and/or is regulated by interactions with non-cardiomyocytes in embryoid bodies (EBs).
View Article and Find Full Text PDFPurpose: The purpose of this study was to reassess whether the Honda sign (HS) and its variants on bone scans can be used to differentiate an insufficiency fracture (IF) of the sacrum from a metastasis and to evaluate extrapelvic tracer accumulation in patients suspected of having a sacral IF.
Methods And Materials: We retrospectively reviewed 34 bone scans of 26 patients suspected of having a sacral IF between January 1998 and June 2003.
Results: Twenty-four of the patients had a sacral IF and 1 had a sacral metastasis from prostate cancer and another from lung cancer.
We previously showed that hyperthermia induced in rhesus monkeys (Macaca mulatta) by forced passive heating "primes" the peripheral lymphocyte population for increased synthesis of interferon-gamma (IFN-gamma). It was not clear whether these data could be extrapolated to the physiological response in naturally occurring fever. Therefore, in the current experiments, the temperature of rhesus monkeys was raised either by systemic injection of killed Escherichia coli or by intrahypothalamic administration of prostaglandin E2.
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