Optimalne potrebe juvenilnih morskih grgeča sebastes schlegeli u proteinima i lipidima

U ovom istraživanju su analizirane optimalne potrebe juvenilnih morskih grgeča Sebastes schlegeli u proteinima i lipidima. 810 juvenilnih riba je izabrano po principu slučajnosti i distribuirano u 27 tankova od po 50 L sa protočnih sistemom. Pripremljeno je 9 eksperimentalnih smeša u vidu 3x3 faktorijalne eksperimentalne postavke: tri nivoa proteina (45, 50 i 55%) x tri nivoa lipida (11, 15 i 19%). Nivo proteina je imao uticaj na prirast riba, dok nivo lipida nije. Prirast riba hranjenih smešom u odnosu 50P-15L (50% proteina i 15% lipida) je bio veći nego prirast riba hranjenih smešama sa 45% proteina, bez obzira na nivo lipida, ali je bio isti kao kod riba hranjenih sa smešama 50P-11L, 50P-19L, 55P-11L, 55P-15L i 55P-19L. Stopa efikasnosti hrane (FER) riba je bila pod uticajem proteina u hrani ali ne i nivoa lipida. Stopa efikasnosti proteina (PER) riba je takođe bila pod uticajem proteina u hrani ali ne i nivoa lipida. Može se zaključiti da je za juvenilne Sebastes schlegeli optimalan nivo proteina i lipida za dobar prirast i iskoristljivost hrane (PER and NRE) 50% i 15% odnosno 45% i 19%, dok je optimalan odnos proteina i energije 27.4 i 23.9 mg protein/kJ

Tau functions as Widom constants

We define a tau function for a generic Riemann-Hilbert problem posed on a union of non-intersecting smooth closed curves with jump matrices analytic in their neighborhood. The tau function depends on parameters of the jumps and is expressed as the Fredholm determinant of an integral operator with block integrable kernel constructed in terms of elementary parametrices. Its logarithmic derivatives with respect to parameters are given by contour integrals involving these parametrices and the solution of the Riemann-Hilbert problem. In the case of one circle, the tau function coincides with Widom's determinant arising in the asymptotics of block Toeplitz matrices. Our construction gives the Jimbo-Miwa-Ueno tau function for Riemann-Hilbert problems of isomonodromic origin (Painlev\'e VI, V, III, Garnier system, etc) and the Sato-Segal-Wilson tau function for integrable hierarchies such as Gelfand-Dickey and Drinfeld-Sokolov.Comment: 26 pages, 6 figure

Effects of C and Al on hydrogen embrittlement mechanism in medium Mn-Ni steels

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Activation of Group I Metabotropic Glutamate Receptors Increases Serine Phosphorylation of GluR1 ␣-Amino-3- hydroxy-5-methylisoxazole-4-propionic Acid Receptors in the Rat Dorsal Striatum

ABSTRACT Protein phosphorylation is an important mechanism for the post-translational modulation of ionotropic glutamate receptors. In this study, we investigated the regulation of ␣-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor GluR1 subunit phosphorylation by the stimulation of group I metabotropic glutamate receptors (mGluRs) in the rat dorsal striatum in vivo. Stimulation of group I mGluRs was found to increase GluR1 phosphorylation of Ser831 and Ser845 in phospholipase C (PLC)-coupled Ca 2ϩ cascades. Interactions of protein kinases activated by intracellular Ca 2ϩ release downstream to PLC modulate the phosphorylation state of GluR1 on Ser831 and Ser845: phosphorylation of GluR1 on Ser831 is up-regulated by the protein kinase C and calcium-calmodulin-dependent protein kinase (CaMK)/c-Jun N-terminal kinase (JNK) pathways, whereas phosphorylation of GluR1 on Ser845 is up-regulated by the protein kinase A (PKA), PKA/ERK1/2, and PKA/JNK pathways. The phosphorylation state of GluR1 on Ser831 and Ser845 and the activity of protein kinases are further regulated by protein phosphatases. These data suggest that GluR1 phosphorylation of Ser831 and Ser845 via stimulation of group I mGluRs is regulated by the interactions of PLC-coupled protein kinases and protein phosphatases in the dorsal striatum. Group I metabotropic glutamate receptors (mGluRs) (mGluR1/5) are densely expressed in the striatum and are colocalized with the majority of either striatonigral or striatopallidal neuron

Toward a Standardized Strategy of Clinical Metabolomics for the Advancement of Precision Medicine

Despite the tremendous success, pitfalls have been observed in every step of a clinical metabolomics workflow, which impedes the internal validity of the study. Furthermore, the demand for logistics, instrumentations, and computational resources for metabolic phenotyping studies has far exceeded our expectations. In this conceptual review, we will cover inclusive barriers of a metabolomics-based clinical study and suggest potential solutions in the hope of enhancing study robustness, usability, and transferability. The importance of quality assurance and quality control procedures is discussed, followed by a practical rule containing five phases, including two additional "pre-pre-" and "post-post-" analytical steps. Besides, we will elucidate the potential involvement of machine learning and demonstrate that the need for automated data mining algorithms to improve the quality of future research is undeniable. Consequently, we propose a comprehensive metabolomics framework, along with an appropriate checklist refined from current guidelines and our previously published assessment, in the attempt to accurately translate achievements in metabolomics into clinical and epidemiological research. Furthermore, the integration of multifaceted multi-omics approaches with metabolomics as the pillar member is in urgent need. When combining with other social or nutritional factors, we can gather complete omics profiles for a particular disease. Our discussion reflects the current obstacles and potential solutions toward the progressing trend of utilizing metabolomics in clinical research to create the next-generation healthcare system.11Ysciescopu

Hypertensive brainstem encephalopathy involving deep supratentorial regions: does only blood pressure matter?

We report on a 42-year-old female patient who presented with high arterial blood pressure of 245/150 mmHg and hypertensive brainstem encephalopathy that involved the brainstem and extensive supratentorial deep gray and white matter. The lesions were nearly completely resolved several days after stabilization of the arterial blood pressure. Normal diffusion-weighted imaging findings and high apparent diffusion coefficient values suggested that the main pathomechanism was vasogenic edema owing to severe hypertension. On the basis of a literature review, the absolute value of blood pressure or whether the patient can control his/her blood pressure seems not to be associated with the degree of the lesions evident on magnetic resonance imaging. It remains to be determined if the acceleration rate and the duration of elevated arterial blood pressure might play a key role in the development of the hypertensive encephalopathy pattern

Role of G{alpha}12 and G{alpha}13 as Novel Switches for the Activity of Nrf2, a Key Antioxidative Transcription Factor

G{alpha}12 and G{alpha}13 function as molecular regulators responding to extracellular stimuli. NF-E2-related factor 2 (Nrf2) is involved in a protective adaptive response to oxidative stress. This study investigated the regulation of Nrf2 by G{alpha}12 and G{alpha}13. A deficiency of G{alpha}12, but not of G{alpha}13, enhanced Nrf2 activity and target gene transactivation in embryo fibroblasts. In mice, G{alpha}12 knockout activated Nrf2 and thereby facilitated heme catabolism to bilirubin and its glucuronosyl conjugations. An oligonucleotide microarray demonstrated the transactivation of Nrf2 target genes by G{alpha}12 gene knockout. G{alpha}12 deficiency reduced Jun N-terminal protein kinase (JNK)-dependent Nrf2 ubiquitination required for proteasomal degradation, and so did G{alpha}13 deficiency. The absence of G{alpha}12, but not of G{alpha}13, increased protein kinase C {delta} (PKC {delta}) activation and the PKC {delta}-mediated serine phosphorylation of Nrf2. G{alpha}13 gene knockout or knockdown abrogated the Nrf2 phosphorylation induced by G{alpha}12 deficiency, suggesting that relief from G{alpha}12 repression leads to the G{alpha}13-mediated activation of Nrf2. Constitutive activation of G{alpha}13 promoted Nrf2 activity and target gene induction via Rho-mediated PKC {delta} activation, corroborating positive regulation by G{alpha}13. In summary, G{alpha}12 and G{alpha}13 transmit a JNK-dependent signal for Nrf2 ubiquitination, whereas G{alpha}13 regulates Rho-PKC {delta}-mediated Nrf2 phosphorylation, which is negatively balanced by G{alpha}12

A collagen gel-coated, aligned nanofiber membrane for enhanced endothelial barrier function

Herein, a collagen gel-coated and aligned nanofiber membrane named Col-ANM is developed, which remarkably improves endothelial barrier function by providing biochemical and topographical cues simultaneously. Col-ANM is fabricated by collagen gel coating process on an aligned polycaprolactone (PCL) nanofiber membrane, which is obtained by a simple electrospinning process adopting a parallel electrode collector. Human umbilical vein endothelial cells (HUVECs) cultured on Col-ANM exhibit remarkably enhanced endothelial barrier function with high expression levels of intercellular junction proteins of ZO-1 and VE-cadherin, a high TEER, and a cellular permeability compared with the artificial porous membranes in commercial cell culture well inserts. The enhanced endothelial barrier function is conjectured to be attributed to the synergistic effects of topographical and biochemical cues provided by the aligned PCL nanofibers and collagen gel in the Col-ANM, respectively. Finally, the reactive oxygen species is applied to the HUVEC monolayer formed on the Col-ANM to destroy the tight junctions between HUVECs. The destruction of the tight junctions is demonstrated by the decreased TEER value overtime. Results indicate the potential of Col-ANM in modeling endothelial barrier dysfunction-related diseases.11Ysciescopu