This study examined the association of problem behavior with neurotransmitter deficiency in adolescents, which would provide new insights into behavioral problems. A total of 1259 students of the seventh grade from 4 middle schools in Wuhan city located in the central China were recruited. With the approval of school and parents, they were invited to complete the Youth Self-Report (YSR) questionnaire and Symptom Scale of Neurotransmitter Deficiency (SSND) questionnaire. Pearson's bivariate correlation analysis showed that the correlation coefficients between each subscale of YSR and SSND ranged from 0.24 to 0.61 with all P<0.01. Canonical correlation analysis indicated that anxiety/depression was interrelated with insufficiency of GABA and 5-HT; aggressive behavior was associated with inadequate GABA; famine of DA influenced the attention problems. It was concluded that neurotransmitter deficiency may cause a series of behavioral and mental problems.
Adolescent ; Adolescent Behavior ; psychology ; Dopamine ; deficiency ; Female ; Humans ; Male ; Mental Disorders ; metabolism ; psychology ; Neurotransmitter Agents ; deficiency ; Serotonin ; deficiency ; Surveys and Questionnaires ; gamma-Aminobutyric Acid ; deficiency

OBJECTIVETo analyze the correlation between changes of thyroid hormone (TH), dopamine (DA) and Chinese medicine syndrome types by detecting contents of serum TH and DA in insomnia, thus to explore objective indices of Chinese medicine syndrome types.

METHODSInsomnia patients were assigned to four Chinese medicine syndrome types groups, covering depressed Gan transforming into fire, internal disturbance by phlegm-heat, excessive fire due to yin deficiency, and Xin-Pi deficiency. One healthy control group was set up. Each group consisted of 30 patients or subjects. Serum DA content was determined using spectrophotofluorometry. Serum levels of 3,5,3'-triiodothyronine (T3) and tetraiodothyronine (T4) were detected using radioimmunoassay (RIA).

RESULTSThe serum levels of DA and TH showed difference among groups at various levels. The serum DA level was sequenced from high to low as the control group > the depressed Gan transforming into fire group > the excessive fire due to yin deficiency group > the internal disturbance by phlegm-heat group > the Xin-Pi deficiency group. The serum TH level was sequenced from high to low as the excessive fire due to yin deficiency group > the depressed Gan transforming into fire group > the internal disturbance by phlegm-heat group > the control group > the Xin-Pi deficiency group.

CONCLUSIONSSerum DA levels in insomnia patients were in line with the disease course and the dynamic change from sthenia to asthenia in Chinese syndrome types. Serum DA levels, as one of pathological factors constituting the sthenia syndrome or the asthenia syndrome, may be taken as an objective indicator in Chinese medicine syndrome typing.

Adolescent ; Adult ; Case-Control Studies ; Diagnosis, Differential ; Dopamine ; blood ; Humans ; Medicine, Chinese Traditional ; Middle Aged ; Sleep Initiation and Maintenance Disorders ; blood ; diagnosis ; Thyroid Hormones ; blood ; Yang Deficiency ; diagnosis ; Yin Deficiency ; diagnosis ; Young Adult

Recently it was shown that single nucleotide polymorphisms (SNPs) can explain individual variation because of the small changes of the gene expression level and that the 50% decreased expression of an allele might even lead to predisposition to cancer. In this study, we found that a decreased expression of an allele might cause predisposition to genetic disease. Dopa responsive dystonia (DRD) is a dominant disease caused by mutations in GCH1 gene. The sequence analysis of the GCH1 in a patient with typical DRD symptoms revealed two novel missense mutations instead of a single dominant mutation. Family members with either of the mutations did not have any symptoms of DRD. The expression level of a R198W mutant allele decreased to about 50%, suggesting that modestly decreased expression caused by an SNP should lead to predisposition of a genetic disease in susceptible individuals.
Child ; Clubfoot/genetics ; Dopamine/deficiency ; Dystonic Disorders/drug therapy/enzymology/*genetics/physiopathology ; GTP Cyclohydrolase/*genetics/metabolism ; Genes, Recessive ; *Genetic Predisposition to Disease ; Humans ; Levodopa/administration & dosage ; Male ; Mutation, Missense ; Pedigree ; Polymorphism, Genetic

Anemia, Iron-Deficiency ; blood ; Area Under Curve ; Dopamine ; metabolism ; Humans ; Hydrocortisone ; blood ; Immunity, Humoral ; Inflammation ; Leukocyte Count ; Lymphocyte Count ; Lymphocytes ; cytology ; Neutrophils ; cytology ; ROC Curve ; Restless Legs Syndrome ; blood ; Sympathectomy ; Time Factors

OBJECTIVETo investigate the toxic effect of environmental neurotoxin MPP+ to C. elegans and identify the mechanisms that cause the toxicity.

METHODSHuman alpha-synuclein transgenic C. elegans was used as the animal model, the toxic effect of MPP+ to dopamine (DA) neurons and the lifespan of worms was tested. The worms were feed with OP50 to determine whether ATP increase can rescue the worm from toxicity. ATP level and aberrant protein accumulation were analyzed in the MPP+ treated worms with or without OP50 addition.

RESULTSWe found that MPP+ induced DA cell death and worm lethality, which could be prevented by OP50 treatment. OP50 exerted the protective effect by up-regulating ATP level, even though it also induced accumulation of alpha-synuclein. Despite the undefined role of protein aggregation to the cell death, our results showed that the toxicity of MPP+ was mainly caused by the ATP depletion in the alpha-synuclein transgenic C. elegans.

CONCLUSIONMPP+ could induce DA neuronal death and worm lethality in alpha-synuclein transgenic C. elegans; Compared with the aggregation of alpha-synuclein, the major cause of MPP+ toxicity appeared due to ATP depletion.

1-Methyl-4-phenylpyridinium ; toxicity ; Adenosine Triphosphate ; deficiency ; metabolism ; Animals ; Animals, Genetically Modified ; Caenorhabditis elegans ; Caenorhabditis elegans Proteins ; drug effects ; metabolism ; Cell Death ; Disease Models, Animal ; Dopamine ; metabolism ; Herbicides ; toxicity ; Humans ; MPTP Poisoning ; metabolism ; mortality ; Neurons ; drug effects ; metabolism ; alpha-Synuclein ; drug effects ; genetics ; metabolism

OBJECTIVETo analyze the clinical characteristics of the patient with tyrosine hydroxylase deficiency, and investigate it's molecular mechanism.

METHODThe clinical characteristics of a patient with tyrosine hydroxylase deficiency were summarized and analyzed, his and his family's peripheral blood specimens were collected after informed consent was signed. All exons and the intron-exon boundaries of guanosine triphosphate hydroxylase I gene, tyrosine hydroxylase gene and sepiapterin reductase gene were examined by DNA-PCR, bi-directional sequencing.

RESULTThe patient was a 3-year-old boy, presented with unexplained dystonia for 3 years, without significant impairment of intelligence. Physical examination showed limb muscle strength grade V, rigidity of extremities, hypertonicity, brisk deep tendon reflexes in limbs, without obvious abnormalities in auxiliary examination, such as brain MRI, hepatic biochemical panel, creatine kinase, and ceruloplasmin. He dramatically responded to small doses of levodopa in the follow-up for half a year. A homozygous missense change in exon 5 of TH gene, c.605G > A (p.R202H), which was a known pathogenic mutation, was found in the patient. His parents were heterozygous for the R202H mutation.

CONCLUSIONThe age of onset in tyrosine hydroxylase deficiency patients is usually within the first year of life. Unexplained dystonia and hypokinesia were the main clinical features of tyrosine hydroxylase deficiency. The dopa-responsive effects for some patients are so obvious that we should strengthen awareness of the disease. TH gene c.605G > A (p.R202H) may be a common type of causative mutations for the mild form at home and abroad.

Brain ; metabolism ; pathology ; Catecholamines ; biosynthesis ; Child, Preschool ; DNA ; genetics ; DNA Mutational Analysis ; Dopamine Agents ; administration & dosage ; therapeutic use ; Dystonic Disorders ; drug therapy ; genetics ; metabolism ; Homozygote ; Humans ; Hypokinesia ; drug therapy ; genetics ; metabolism ; Levodopa ; administration & dosage ; therapeutic use ; Male ; Muscle Rigidity ; drug therapy ; genetics ; metabolism ; Mutation, Missense ; Polymerase Chain Reaction ; Tyrosine 3-Monooxygenase ; deficiency ; genetics ; metabolism