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Copyright of Chinese Journal of Bioprocess Engineering is the property of Chinese Journal of Bioprocess Engineering Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The anti-exercise-fatigue effect of active peptides derived from fish nicotinamide adenine dinucleotide Dehydrogenase (NADH) was investigated by simulating the hydrolysis of NADH Dehydrogenase protein subunits in five common fish species in China using computer simulations. The oligopeptides obtained through simulated hydrolysis were docked with lactate Dehydrogenase (LDH) and creatine kinase (CK) to identify the oligopeptides with ultra-high affinity for both enzymes (docking fraction ≤ -160), whereas Pymol and Ligplot+ software were used to display and analyze the mechanisms of interaction for molecular docking. The results showed that a total of 72 oligopeptides with ultra-high affinity were obtained from seven different NADH Dehydrogenase protein subunits of five fish species after computer-simulated hydrolysis and molecular docking. There were 36 oligopeptides with ultra-high affinity for LDH and CK, among which the oligopeptide with the highest docking score and the most frequent occurrence was PTIW (-198.762, -204.400). These results establish a theoretical foundation for improving the high-value utilization of fish protein and developing functional foods for anti-exercise-fatigue. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Preventive Veterinary Medicine / Zhongguo Yufang Shouyi Xuebao is the property of Chinese Journal of Preventive Veterinary Medicine Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of South China Fisheries Science is the property of South China Fisheries Science Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Shipin Kexue/ Food Science is the property of Food Science Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Shipin Kexue/ Food Science is the property of Food Science Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Shipin Kexue/ Food Science is the property of Food Science Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of South China Fisheries Science is the property of South China Fisheries Science Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Leber hereditary optic neuropathy (LHON) is a mitochondria hereditary eye disease that involves with retinal ganglion cells (RGCs) resulting eventually in degeneration and atrophy of optic nerve. The three mitochondrial DNA mutations (ND4 G11778A, ND1G3460A, ND6T14484C) have been recognized as the primary mutation locus of LHON. Currently there is no effective therapy for LHON. The result of a clinical trial launched in 2007 indicated that intraocular injection of the recombination of adeno-associated virus and target gene is an effective and safe cure for Leber's Congenital Amaurosis (LCA), which brings hope of treating other hereditary eye diseases with gene therapy. Since LHON mainly involves with RGCs, the target gene can be delivered directly to RGCs with the means of injecting the recombination into vitreous cavity, therefore resulting in less damage to retina as compared to other gene therapy for LCA which require the drug to be injected under the retina. This article summarizes the research progress of the clinical trial relevant to gene therapy for LHON. (Chin J Ophthalmol, 2018, 54: 636-640) .

Objective: To analyze the clinical and genetic features of progressive cavitating leukoencephalopathy (PCL). Method: The data of clinical and genetic features of 4 PCL patients diagnosed by Beijing Children's Hospital between January 2015 and January 2016 were analyzed. The cases with complete clinical data retrieved on literature search at China National Knowledge Infrastructure, Wanfang Data Knowledge Service Platform and PubMed (up to August 2016) by using search terms of"NDUFV1" ,"NDUFS1" , or"leukoencephalopathy" , were summarized. Result: There were three females and one male, two of which were compatriots. The age of onset ranged from 6 months to 15 months. All four children's first symptoms were motor development regression, and the developmental milestones were almost normal before the onset. Of the 4 patients, 3 had cognitive impairment, 1 had seizures, 4 had dystonia and pyramidal impairment, 2 had emaciation, and 1 had nystagmus. The lactate concentrations of 4 patients were normal in blood. One patient had lactaciduria in the urinary organic acid analysis. Cranial magnetic resonance imaging (MRI) of all patients showed leukoencephalopathy, involved in the corpus callosum, and three patients accompanied by cystic lesions. Follow up for 2-13 years showed that the physical and language development were improved. Genetic analysis revealed that mutations in NDUFS1 were found in three patients and NDUFV1 mutation was found in one patient. All six mutations (p.Arg377Cys and p. Arg377His in NDUFV1; p. Arg482Glyfs(*)5, p.Thr368Pro, p.Tyr454X and p. Asp565Gly in NDUFS1) are novel. Five English case reports including 10 PCL patients were collected. Together with this group of 4 cases, a total of 14 cases were involved. All 14 children patients had motor development regression, 11 cases had cognitive impairment and dystonia, 6 cases had pyramidal impairment, 5 cases had irritability, 4 cases had epilepsy and nystagmus, 3 cases had strabismus and swallowing difficulty. Cranial MRI showed patchy leukoencephalopathy with cavities, involved in the corpus callosum. Follow up for 19 months-15 years that the neurology development were improved slowly in all patients. Conclusion: NDUFS1 and NDUFV1 gene mutation screening should be performed firstly in patients with PCL clinical and imaging feature.