The present invention relates to a method for generating sterile Zeugodacus scutellata males by emitting an electron beam at a dose of 150 Gy (inclusive) to 250 Gy (exclusive) to pupae of Zeugodacus scutellata and a method for controlling Zeugodacus scutellata by releasing the generated sterile males and normal males at a ratio of 9:1. In the present invention, electron beams are used instead of radioactive beams and suitable doses of electron beams are determined to generate sterile males of domestic native Zeugodacus scutellata. The generated sterile Zeugodacus scutellata males and normal males are released at a ratio of 9:1 to effectively control Zeugodacus scutellata through a sterile insect release technique (SIT).

Provided is a method for preparing a diabetic dog model by means of gene editing technology, a diabetic dog model prepared therefrom, as well as cells and issues thereof. The method comprises the following steps: (1) obtaining a dog fertilized egg cell, which comprises a point mutation in GCK gene, for a diabetic dog model by means of gene editing; and (2) transplanting the dog fertilized egg cell into one fallopian tube of a female dog, in which both fallopian tubes have been flushed, to prepare a diabetic dog model comprising a point mutation in GCK gene.

The present disclosure relates generally to the field of immunotherapy. In particular, the present disclosure describes to 20 single nucleotide variants (SNVs) within the A20 coding sequence that can differentially impact the immune system. Differential expression of the identified A20 SNVs can be used to “tune” the immune system of a subject e.g., tune up or tune down the sensitivity and/or strength of the immune system of a subject in response to a treatment or a pathogen. On the basis, the present disclosure provides methods for modulating the immune system of a subject by modulating the A20 SNV expression profile in the subject, thereby “tuning” the immune system. The present disclosure also describes reagents for use in such methods. The methods and reagents may have application in the treatment and/or management of diseases/conditions such as, for example, cancer, autoimmune disease, pathogenic infection, complement deficiency, and transplant rejection, where the strength of a subject's immune system plays an important role. The present disclosure also describes methods in which the A20 SNVs are used as biomarkers to stratify subjects according to the strength of their immune system e.g., strong or poor immune response relative to a reference A20 genotype, and the use of such methods in personalised medicine.

Provided, inter alia, are methods and compositions for treating epilepsy. In one aspect, provided herein is a method of selecting a compound for treating epilepsy, said method includes, contacting a test compound with 5-hydroxytryptamine-2B receptor (5-HT2B), and measuring the 5-HT2B agonistic activity of the test compound. In another aspect, provided herein is a method of treating an epilepsy in a subject in need thereof. The method includes administering to said subject an effective amount of a 5-HT2B specific receptor agonist.

Provided is a nonhuman animal model that is obtained by modifying a gene encoding thioredoxin and useful as a disease model of aging, kidney diseases, cardiovascular diseases, hypertension, aortic dissection, chronic obstructive lung disease, age-dependent epilepsy, abnormality of lipid metabolism, anemia, osteoporosis, abnormal immunity, etc. These variety of phenotypes are caused by the fact that a modification of a gene encoding thioredoxin induces hypofunction of thioredoxin expressed in multiple organs throughout the body. The gene encoding thioredoxin is a gene selected from among TXN, TRX, TRX1, RRDX, Txn1, Txn, Trx1 and ADF.

The present disclosure relates generally to methods of treating a subject having muscular dystrophy or DMD. The present disclosure also relates generally to methods of prophylactically treating a subject at risk of developing muscular dystrophy or DMD. In some embodiments, the methods may include administering a pharmaceutical composition including an RRM1 gene, an RRM2 gene, and a delivery vehicle to a subject. In another embodiment, the methods may include administering a pharmaceutical composition including an RRM1 gene and an RRM2 gene coupled to a regulatory cassette to a subject. In yet another embodiment, the methods may include administering a pharmaceutical composition including an RRM 1 gene, an RRM2 gene, a regulatory cassette, and a delivery vehicle to a subject.

Method for producing YY super-male and XY physiological female common carps, with which YY-chromosome super-male common carp can be cultivated and androgenetic YY super-male common carp is produced, where microsatellite markers are used for paternity testing and test crossing confirmation. The YY common carp is crossed with normal female common carp to produce the progenies of only male common carp, and without sex identification, the juvenile male common carp with known sex are subjected to artificial sex reversal to produce XY physiological female common carp.

Compositions and methods for attenuating or preventing lymphoproliferation in a subject are provided. The subject may have, be suspected of having, or at risk of having a lymphoproliferative disease. The methods herein include administering to the subject a composition effective for decreasing WD repeat domain protein 37 (Wdr37) expression and/or activity.

One variation of a method includes: at a feeder module, subjecting a first set of cages to a first set of environmental conditions configured to promote deposition of fly eggs by adult flies, each cage, in the first set of cages, containing a fly population, in a set of fly populations, genetically modified to generate amounts of a target compound; at an incubator module, subjecting a second set of cages to a second set of environmental conditions configured to promote transformation of fly eggs into fly larvae; at a treatment module, subjecting a third set of cages to a third set of environmental conditions configured to promote generation of a target compound in fly larvae contained within the third set of cages; and, at a repopulation module, subjecting a fourth set of cages to a fourth set of environmental conditions configured to promote transformation of fly larvae into adult flies.

Inappropriate activation of innate immune responses in nematode intestinal epithelial cells underlies the pathophysiology of some inflammatory disorders. Immunostimulatory xenobiotics are known to protect nematodes from bacterial infection (e.g., Pseudomonas aeruginosa). Conversely, these same xenobiotics are toxic to uninfected nematodes. These xenobiotics were subjected to a forward genetic screen in uninfected nematodes to identify nematode mutants that were resistant to the deleterious effects of these xenobiotics. These resistant nematode strains contained hypomorphic mutations in each of the known components of the p38 MAP kinase cassette (tir-1, nsy-1, sek-1 and pmk-1), demonstrating that hyperstimulation of p38 MAPK innate immune responses may be responsible for the induced toxicity. A second genetic screen using dominant activators of the p38 MAPK pathway identified a single allele that had a gain-of-function (gf) mutation in nsy-1, the MAP kinase kinase kinase that acts upstream of p38 MAPK pmk-1.