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1.
Transl Psychiatry ; 9(1): 275, 2019 Nov 07.
Article in English | MEDLINE | ID: mdl-31699979

ABSTRACT

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

2.
Transl Psychiatry ; 9(1): 40, 2019 01 29.
Article in English | MEDLINE | ID: mdl-30696813

ABSTRACT

The gut microbiota has been increasingly correlated with depressive disorder. It was recently shown that the transplantation of the gut microbiota from depressed patients to animals can produce depressive-like behaviors, suggesting that the gut microbiota plays a causal role in the development of depression. In addition, metabolic disorder, which is strongly associated with depression, is exacerbated by changes in the composition of the gut microbiota and is alleviated by treatment with antidepressants. However, the key players and pathways that link the gut microbiota to the pathogenesis of depression remain largely unknown. To evaluate the relationships between depression and metabolic disorders in feces and plasma, we monitored changes in fecal and plasma metabolomes during the development of depressive-like behaviors in rats exposed to chronic unpredictable mild stress (CUMS). In these animals, the fecal metabolome was altered first and subjected to changes in the plasma metabolome. Changes in the abundance of fecal metabolites were associated with depressive-like behaviors and with altered levels of neurotransmitters in the hippocampus. Furthermore, the analysis of the fecal metabolome and the fecal microbiota in CUMS rats demonstrated consistent changes in the levels of several amino acids, including L-threonine, isoleucine, alanine, serine, tyrosine, and oxidized proline. Finally, we observed significant correlations between these amino acids and the altered fecal microbiota. The results of this study suggest that changes in amino acid metabolism by the gut microbiota contribute to changes in circulating amino acids and are associated with the behavior indices of depression.


Subject(s)
Depression/metabolism , Depression/microbiology , Feces , Gastrointestinal Microbiome , Stress, Psychological/complications , Animals , Behavior, Animal , Depression/etiology , Feces/microbiology , Male , Metabolome , Rats, Sprague-Dawley
3.
Article in Zh | WPRIM | ID: wpr-827713

ABSTRACT

Waardenburg syndrome (WS), also known as auditorypigmentary syndrome, is characterized by non-progressive sensorineural hearing loss and anomalous pigmentation. Its mode of inheritance is either autosomal dominant or autosomal recessive. So far only PAX3, MITF, SOX10 and EDNRB mutations have been identified among Chinese patients with WS. This review has provided an update for WS-related genes, mutation databases, molecular and functional data, and a discussion over the molecular diagnosis of WS.

4.
Sci China C Life Sci ; 47(1): 25-30, 2004 Feb.
Article in English | MEDLINE | ID: mdl-15382673

ABSTRACT

Myostatin, a new member of the TGF-beta superfamily, is predominantly expressed in skeletal muscle cells and functions as a negative regulator of skeletal muscle growth in animals. Recently, we have reported three single nucleotide polymorphisms (SNPs) in the chicken myostatin gene. Herein, we investigate the association of those SNPs with the production traits in a F2 chicken line derived from Broilers crossing to Silky with the least square analysis. The results show that the BB and AA genotypes are strongly associated with abdominal fat weight (AFW), abdominal fat percentage (AFP), and birth weight (BW) (P < 0.05). Breast muscle percentage (BMP) of the AA type is higher than that of the AB type. The breast muscle weight and breast muscle percentages of F2 individuals have significant difference between CC and DD genotypes (P< 0.05). Breast muscle weight (BMW) of EF birds is higher than that of EE birds (P< 0.05). In this report, we present the first genetic evidence to show that chicken myostatin not only plays an important role in controlling skeletal muscle growth and differentiation, but also may be involved in regulation of adipose growth in chicken.


Subject(s)
Adipose Tissue/growth & development , Chickens/growth & development , Chickens/genetics , Muscle, Skeletal/growth & development , Polymorphism, Single Nucleotide , Transforming Growth Factor beta/genetics , Animals , Base Sequence , Crosses, Genetic , DNA/genetics , Female , Genotype , Male , Myostatin , Phenotype
5.
Chinese Journal of Zoonoses ; (12): 403-412, 2017.
Article in Zh | WPRIM | ID: wpr-620066

ABSTRACT

We detected the isoniazid resistance in clinical Mycobacterium tuberculosis isolates by high-resolution melting (HRM) curve analysis and assessed the application value of the assay.The isoniazid resistance of 49 M.tuberculosis isolates preserved in laboratory was analyzed by the drug sensitivity test (traditional proportion method).Further analysis was made on the sequencing of the isoniazid resistance determining region in these test strains,and their mutation sites were screened.Specific primers used in the HRM curve analysis were designed based on the screened mutation sites,DNA mutations were assayed in the isoniazid-resistant gene determining region by the HRM curve analysis,and an assessment was made of the detection efficiency of the assay in isoniazid resistance in M.tuberculosis.Results of the drug sensitivity test (proportion method) showed that,of the 49 test strains,there were 20 isoniazid-resistant strains,29 isoniazid-sensitive strains.Results of the sequencing analysis showed that:1) KatG gene had four mutation patterns,i.e.,point mutations at site 234,at sites 234 and 315,at sites 234 and 463,and at sites 234,315 and 463;2) there were three mutations were detected in inhA gene,i.e.,mutations in inhA-8,-15 and-152.Analysis of gene mutation in drug-resistant strains found that of the 20 isoniazid-resistant strains,11 (55 %) were mutated at codon 315 of KatG gene;6 (30%) were mutated in inhA-15 (4/20),-8 (1/20) and-153 (1/20) of inhA gene;two (10%) were mutated at codon 315 of KatG gene and in inhA-15;in one strain (5%),no mutation was detected in KatG and inhA genes.Through the gene mutation detection,the sensitivity and specificity of isoniazid resistance in M.tuberculosis were 95 % and 100 %,respectively.Results of HRM curve analysis of drug-resistance gene mutations in test strains showed gene mutations were present in 18 strains and absent in 24 ones;referring to DNA sequencing results,the sensitivity and specificity of the assay were 94.7% and 80%,respectively.Judged by mutations as drug-resistance via the HRM curve analysis,19 resistant and 24 sensitive strains were tested.With the drug sensitivity test results by the proportion method as controls,the sensitivity and specificity of the assay were 95 % and 82.76 %,respectively.Use of the HRM curve in the detection of resistance of M.tuberculosis to isoniazid is characterized by good sensitivity and short time consuming,and has certain value in the rapid diagnosis of isoniazid-resistant tuberculosis.

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