Abstract: The present disclosure discloses a method, product, and system for cogenerating ferric phosphate through a nitrophosphate fertilizer device. The method comprises the steps of: acid-hydrolyzing phosphate rock with a nitric acid, and separating acid-insoluble substances to obtain an acid-hydrolyzed solution; freezing-crystallizing the acid-hydrolyzed solution, and carrying out solid-liquid separation to obtain a first solution; adding a solution containing sulfate ions to the first solution for reaction to obtain a second solution; subjecting the second solution to a denitrification to obtain a third solution; adding ammonia to the third solution for neutralization, and carrying out solid-liquid separation to obtain an ammonium phosphate solution, and adding an iron source to the ammonium phosphate solution for reaction to prepare a ferric phosphate.

Abstract: The present disclosure relates to the technical field of ferric phosphate, in particular to a process and a system for preparing ferric phosphate by mixing and stirring in a reactor with external circulation. Disclosed is a process for preparing ferric phosphate by mixing and stirring in a reactor with external circulation, comprising the following steps: adding a ferric salt solution, a monoammonium phosphate solution, and a protective agent into the reactor, and subjecting the resulting mixed liquid to a preliminary reaction at 90-100° C.; after the completion of the preliminary reaction, carrying out an external circulation reaction at 85-90° C. The process described in the present disclosure has a high reaction speed, and the obtained ferric phosphate has a high yield and low content of impurity in the ferric phosphate.

Abstract: The present invention relates to the engineering an animal model, preferably mammalian models, more preferably a rat model representing Charcot-Marie-Tooth disease 2A (CMT2A) harboring the p.Arg364Trp or p.His361Tyr Mfn2 mutation, whose human counterpart results in a severe, early-onset axonal neuropathy. A model having the p.Arg364Trp Mfn2 mutation is based on a mutation made using zinc finger endonuclease technology in fertilized rat eggs. Cohorts of mutants and wild type littermates were characterized behaviorally and shown to develop multiple motor deficits that worsened over time. Separate cohorts of mutant and wild type rats sacrificed at 7, 40, and 48 weeks and analyzed by light microscopy showed a reduced density of myelinated axons and active axonal degeneration in distal but not proximal nerves, as well as axonal degeneration in the fasciculus gracilis of the cervical spinal cord at 40 and 48 weeks.

Abstract: Disclosed is a method for preparing iron phosphate and by-product fertilizer using ammonium phosphate. The granulation device for by-product fertilizer production comprises a housing having accommodation space which is divided from top to bottom into a granulation chamber, a material-screening chamber and a temporary material-storing chamber; a blowing component provided between the granulation chamber and the material-screening chamber; and a vibrating screen which is able to vertically reciprocated provided between the material-screening chamber and the temporary material-storing chamber which is connected to a discharge pipe, wherein the upper end of the housing is provided with a detachable cover having multiple spraying devices for spraying the molten material into the housing and connected to an exhaust pipe.

Abstract: The present invention relates to Charcot-Marie-Tooth disease 2A (CMT2A) harboring the p.Arg364Trp or p.His361Tyr Mfn2 mutation, whose human counterpart results in severe, early-onset axonal neuropathy for p.Arg364Trp Mfn2 mutation in fertilized rat eggs. Cohorts of mutants and wild type littermates were characterized with multiple motor deficits that worsened over time. Separate cohorts of mutant and wild type at 7, 40, and 48 weeks showed reduced density of myelinated axons and active axonal degeneration in distal but not proximal nerves, as well as axonal degeneration in the fasciculus gracilis of the cervical spinal cord at 40 and 48 weeks not present in 7-week-old cohort Mfn2 mutants, or wild type at 7 or 40 weeks. The p.His361Tyr Mfn2 mutation using CRISPR/Cas9 showed abnormalities in gait dynamics at 8 weeks and lengthening of gait cycle at 16 weeks. The invention provides progressive axonal neuropathy for examining pathogenesis and treatment of CMT2A.

Abstract: The present invention relates to the engineering an animal model, preferably mammalian models, more preferably a rat model representing Charcot-Marie-Tooth disease 2A (CMT2A) harboring the p.Arg364Trp or p.His361Tyr Mfn2 mutation, whose human counterpart results in a severe, early-onset axonal neuropathy. A model having the p.Arg364Trp Mfn2 mutation is based on a mutation made using zinc finger endonuclease technology in fertilized rat eggs. Cohorts of mutants and wild type littermates were characterized behaviorally and shown to develop multiple motor deficits that worsened over time. Separate cohorts of mutant and wild type rats sacrificed at 7, 40, and 48 weeks and analyzed by light microscopy showed a reduced density of myelinated axons and active axonal degeneration in distal but not proximal nerves, as well as axonal degeneration in the fasciculus gracilis of the cervical spinal cord at 40 and 48 weeks.

Abstract: An inactive CRISPR/Cas system-based fusion protein and its applications in gene editing are disclosed. More particularly, chimeric fusion proteins including an inCas fused to a DNA modifying enzyme and methods of using the chimeric fusion proteins in gene editing are disclosed. The methods can be used to induce double-strand breaks and single-strand nicks in target DNAs, to generate gene disruptions, deletions, point mutations, gene replacements, insertions, inversions and other modifications of a genomic DNA within cells and organisms.

Abstract: The present invention provides a method of determining the status of a multiple sclerosis patient, i.e., predicting the transition from a status of relapsing-remitting to a progressive phase of multiple sclerosis, comprising the step of measuring the amount of urinary p-cresol sulfate in the patient. The present invention also provides a method of determining the amount of lesions and total lesion area of a multiple sclerosis patient, comprising the step of measuring the amount of urinary p-cresol sulfate in the patient. Further provided is a method of monitoring myelination in a developing child, comprising the step of: measuring the amount of p-cresol sulfate in the urine of said child.

Abstract: The present invention provides a method of determining the status of a multiple sclerosis patient, i.e., predicting the transition from a status of relapsing-remitting to a progressive phase of multiple sclerosis, comprising the step of measuring the levels of urinary myelin basic protein-like material in the patient. The present invention also provides a method of determining the amount of lesions and total lesion area of a multiple sclerosis patient, comprising the step of measuring the levels of urinary myelin basic protein-like material in the patient. Further provided is a method of monitoring myelination in a developing child, comprising the step of: measuring the levels of myelin basic protein-like material in the urine of said child.