47 results about "Neural tube defect" patented technology

Maternal diabetes suppresses autophagy in neuroepithelial cells of the developing neural tube which leads to neural tube defect formation. Trehalose treatment reversed autophagy impairment and prevented neural tube defects in diabetic pregnancies. Trehalose resolved homeostatic imbalance by correcting mitochondrial defects, dysfunctional proteins, ER stress, apoptosis, and delayed neurogenesis in the neural tubes exposed to hyperglycemia. Methods of using trehalose as an intervention against hyperglycemia-induced neural tube defects are provided herein.

The invention features a novel gene encoding methionine synthase reductase. The invention also features a method for detecting an increased likelihood of hyperhomocysteinemia and, in turn, an increased or decreased likelihood of neural tube defects, cardiovascular disease, Down's Syndrome or cancer. The invention also features therapeutic methods for treating and / or reducing the risk of cardiovascular disease, Down's Syndrome, cancer, or neural tube defects. Also provided are the sequences of the human methionine synthase reductase gene and protein and compounds and kits for performing the methods of the invention.

The invention provides a method for obtaining a mouse model with neural tube defects (NTDs). The mouse model with the NTDs is established by applying an anti-inositol metabolism medicament to a pregnant mouse from the embryonic development of the pregnant mouse to the formation of neural tubes. The mouse model can be used for medical and biological research of the NTDs, is helpful to understand the causes and pathogenesis of human NTDs, and provides a model for further research on an action mechanism of inositol metabolic disorders in the NTDs. Moreover, according to the method, the neural tube defect rate is high, absorbed embryos are few, the embryo fatality rate is low, and toxic and side effects to the pregnant mouse are low.

The present invention provides a method for isolating human neural stem cells from amniotic fluid of a patient whose fetus has been diagnosed to have a neural tube defect. Use of the isolated human neural stem cells in the treatment of neurological disorders is also provided.

The invention relates to an application of antifolic in constructing a mouse model with neural tube defects (NTDs). Specifically, an anti-folic acid metabolism drug is adopted for intervening a pregnant mouse to generate folic acid dysbolism and cause abnormal embryonic development of the mouse, thereby constructing a mouse model with NTDs. The method adopted by the invention has simplicity of operation, good repeatability, high teratogenesis rate and stable effect, and simulates an animal model close to human on the pathogenesis of NTDs by obstructing normal metabolism of folic acid, thereby facilitating further studies on congenital anomalies, especially NTDs.

The invention discloses a method for screening open neural tube defects (ONTD) of fetuses through maternal serum alpha-fetoprotein heteroplasmons L2 and L3 in a second trimester. The method comprisesthe following steps: (1) forming a case group by multiple pregnant women with fetuses determined as ONTD fetuses through ultrasonic tomography, and randomly forming a control group through multiple pregnant women with fetuses who grow normally; (2) detecting the levels of AFP-L2 and AFP-L3 of serums of two groups of the pregnant women by virtue of ELISA, carrying out statistical treatment on the correlation between the levels of AFP-L2 and AFP-L3 of the serums of the pregnant women in the second trimester and the ONTD of the fetuses, and analyzing the screening efficiency by virtue of different constructed risk calculation models; and (3) calculating the optimal critical values and areas under the curve of AFP-L2 and AFP-L, for screening the ONTD fetuses, of the serums of the pregnant women. The method has the beneficial effects that AFP-L2 and AFP-L of the serums of the pregnant women in the second trimester have relatively high sensitivity and specificity to the screening of the ONTDfetuses and are relatively good markers for screening the ONTD, and the screening efficiency of the risk calculation model constructed by virtue of AFP-L2 and AFP-L3 is better than that of an MoM value respectively corresponding to AFP, AFP-L2 and AFP-L3.

The present invention identifies autoantibodies to folate receptors. Methods to identify these autoantibodies to the human folate receptors are also provided. The present invention also contemplates diagnostic methods and test kits to be used in a clinical setting for identifying a subject at risk of folate-sensitive abnormalities or disorders as observed in neural tube defect complicated pregnancies. In addition, infertility, spontaneous abortion, male sterility, unsuccessful in vitro fertilization, neurologic disorders and impaired folate absorption may also be associated with these autoantibodies to folate receptors.

The present invention relates to a pharmaceutical composition which comprises progestogens, preferably drospirenone, estrogens, preferably ethinylestradiol and 5-methyl-(6S)-tetrahydrofolate, can be employed as oral contraceptive and moreover prevents disorders caused by folate deficiency in the consumers, in particular cardiovascular disorders and, after conception of the embryo, congenital malformations caused by folate deficiency such as, for example, neural tube defects, ventricular valve defects, urogenital defects, and cleft lip, jaw and palate, without masking the symptoms of vitamin B12 deficiency, and at the same time even in the case of homozygous or heterozygous polymorphism of methylenetetrahydrofolate reductase facilitates unimpaired utilizability of the folate component 5-methyl-(6S)-tetrahydrofolate by the body and thus its biological activity for preventing the abovementioned congenital malformations caused by folate deficiency. In addition, a prolonged protective effect is maintained after discontinuation of the contraceptive.

The invention relates to the field of applied basic medical research, in particular to a method for constructing a neural tube defect mouse model. The present invention uses physical or chemical teratogenic factors to intervene pregnant mice fed with a low folic acid diet, uses low folic acid as a sensitizing factor, imitates the human physiological environment, induces neural tube defects in mice, and greatly increases the success rate of model construction; The method adopted in the invention is simple, has good repeatability, high deformity rate, little toxic and side effects in pregnant mice, and low embryo lethality rate.

The invention discloses a method for constructing a neural tube defect model, which comprises the following steps: step 1, collecting artificially inseminated eggs, cleaning them and placing them in an incubator for incubation; step 2, incubating the eggs to the neural plate of chicken embryos After the start of closure, inject homocysteine ​​thiolactone into the eggs using the chicken embryo neural groove injection method; step 3, continue to incubate the treated eggs, observe the phenotype of the chicken embryos, and screen out successful neural tube defects Model. Another aspect of the present invention also discloses the application of the above construction method in the study of the pathogenesis of neural tube defects caused by high homocysteine. By adopting the neural tube defect model construction method provided by the invention, the deformity rate of the nervous system reaches 50%, and the embryo survival rate reaches 87.5%, which is currently the best modeling method for observing neural tube defects.

The invention offers oligonucleotide adapter of specific combining human-brain acetylcholinesterase containing SEQ ID: 1, SEQ ID: 2 or SEQ ID: 3 sequence, method of detecting or discriminating human-brain acetylcholinesterase, method and diagnostic reagent and medicine to diagnose or therapy the disease relating to human-brain acetylcholinesterase (especially neural tube defect and neurotic disorder), and so on.