Fragility and robustness of self-sustained oscillations in an epidemiological model on small-world networks.

We investigate the susceptible-infected-recovered-susceptible epidemic model, typical of mathematical epidemiology, with the diversity of the durations of infection and recovery of the individuals on small-world networks. Infection spreads from infected to healthy nodes, whose infection and recovery periods denoted by τI and τR, respectively, are either fixed or uniformly distributed around a specified mean. Whenever τI and τR are narrowly distributed around their mean values, the epidemic prevalence in the stationary state is found to reach its maximal level in the typical small-world region. This non-monotonic behavior of the final epidemic prevalence is thought to be similar to the efficient navigation in small worlds with cost minimization. Besides, pronounced oscillatory behavior of the fraction of infected nodes emerges when the number of shortcuts on the underlying network become sufficiently large. Remarkably, we find that the synchronized oscillation of infection incidences is quite fragile to the variability of the two characteristic time scales τI and τR. Specifically, even in the limit of a random network (where the amplest oscillations are expected to arise for fixed τI and τR), increasing the variability of the duration of the infectious period and/or that of the refractory period will push the system to change from a self-sustained oscillation to a fixed point with negligible fluctuations in the steady state. Interestingly, negative correlation between τI and τR can give rise to the robustness of the self-sustained oscillatory phenomenon. Our findings thus highlight the pivotal role of, apart from the external seasonal driving force and demographic stochasticity, the intrinsic characteristic of the system itself in understanding the cycle of outbreaks of recurrent epidemics.

[Genome-wide search for linkage to attention deficit hyperactivity disorder (ADHD) on the X chromosome].

Attention deficit hyperactivity disorder (ADHD) is the most common childhood-onset behavioral. Boys are more often affected than girls. Family, twin and adoption studies have supported a strong genetic basis. The etiology of this disorder is not clear. Molecular genetic and pharmacological studies suggest the involvement of dopaminergic and noradrenergic neurotransmitter systems in ADHD, e.g , Several reports have found association between ADHD and the dopamine receptor gene DRD-4.the dopamine transporter gene DAT1, and the catechol-o-methyltransferase. Our previous studies showed an association between ADHD and the DXS7 locus, which is located in closely linked to the MAO gene, and MAOA gene on chromosome X. To test this hypothesis, we used the genome scan for a predisposing locus on chromosome X to ADHD. We used the tramsmission/disequilibrium test (TDT) to test for linkage between a VNTR polymorphism at the 48 markers of chromosome X and DSM-III-R oliagnosed ADHD in 84 nuclear families of the Chinese population. The TDT analysis revealed linkage between ADHD and the DXS1214(TDT: Chi2=18.1, df=7, P<0.01), DXS8102(TDT: Chi2=7.9, df=3, P<0.05), DXS1068(TDT: Chi2=21.9, df=9, P<0.01), DXS8015(TDT: Chi2=14.6, df=7, P<0.05), DXS1059(TDT: Chi2=27.8, df=10, P<0.01) and DXS8088(TDT: Chi2=20.4, df=3, P<0.01).The data showed that susceptibility loci might reside in chromosome Xp11.4-Xp21 and Xq23 for ADHD.

No association between attention-deficit hyperactivity disorder and catechol-O-methyltransferase gene in Chinese.

Previous studies suggested that the catecholaminergic systems may be involved in the pathogenesis of attention-deficit hyperactivity disorder(ADHD). Since catechel-O-methyltransferase (COMT) is an enzyme involved in the degradation of catecholaminergic neurotransmitters of the dopaminergic and noradrenergic systems,it is possible that COMT may play a role in ADHD. To test this hypothesis, we used two family-based analyses,the transmission disequilibrium test (TDT) and the haplotype-based haplotype relative risk (HHRR), to examine the possible association between COMT gene and DSM-IV-diagnosed ADHD in a Chinese sample consisting of 79 ADHD probands and their parents. Both TDT (chi2 = 1.03, df=1, P > 0.05) and HHRR (chi2 = 1.08, df = 1, P > 0.05) analyses failed to detect preferential transmission of a COMT allele to the ADHD children. Our data suggested that there was no association between ADHD and the COMT gene in the Chinese population.

[A pedigree with myotonic dystrophy: non-CTG, non-CCTG repeat expansion].

OBJECTIVE: Two genetic loci are associated with the myotonic dystrophy (DM) phenotype: DM1 DMPK on chromosome 19, and DM2 ZNF9 on chromosome 3. The aim of this study was to investigate the molecular genetics of a pedigree with DM. METHODS: In twenty-six individuals from a family with DM, the CTG repeats in DMPK and CCTG repeats in ZNF9were evaluated genetically, using Long Expand trade mark Template polymerase chain reaction (PCR), Southern blotting and genomic scanning. RESULTS: The numbers of CTG and CCTG repeat were all in normal range. There was no significant difference between the CTG repeat size in DMPK gene and that 4 years later from the same individual. The Lod score values with short tandem repeats STR markers chosen in 19q and 3q were all smaller than 1, which suggested that no STR marker was linked with this DM family. CONCLUSION: There might be some other mutant in this DM pedigree. Further study should be done to find the genetic basis of this pedigree.

[Study on gamma-synuclein gene in patients with idiopathic Parkinson's disease].

OBJECTIVE: To evaluate the relationship between idiopathic Parkinson's disease (PD) and two polymorphisms (C243G and A377T) of the gamma-synuclein gene in a Chinese Han population of Shanghai area. METHODS: Polymorphic genotyping was performed with PCR-RPLP technique. Association analysis was carried out in 145 unrelated idiopathic PD patients and 184 age-matched healthy controls. RESULTS: The authors failed to detect any distributional difference of the C243G and A377T polymorphisms of the gamma-synuclein gene between PD cases and control subjects, nor did they find any association. CONCLUSION: These data do not support that gamma-synuclein gene C243G and A377T polymorphisms are involved in idiopathic PD onset in the Han population of Shanghai area.

[Dopamine beta hydroxylase gene polymorphism and Parkinson's disease].

OBJECTIVE: To investigate the correlation between the polymorphism of dopamine beta hydroxylase(DBH) gene and the susceptibility of Shanghai Chinese Han population to Parkinson's disease(PD). METHODS: Association study was performed in 144 PD patients and 188 healthy control subjects matched for age, sex and origin. Polymorphism of DBH gene was analyzed with polymerase chain reaction-restriction fragment length polymorphism. RESULTS: The allelic frequency of A2 allele of DBH gene was significantly higher in PD patients than in controls(P<0.01).The risk of suffering from PD increased (OR=1.82) in the individual with A2 allele. And the genotypic frequency of A2/A2 was significantly higher in PD patients(OR=2.11, P<0.01),too. On the other hand, the allelic frequency of A1 allele and the genotypic frequency of A1/A2 genotype of DBH gene in PD patients were significantly lower(A1 alleles: OR=0.54, P<0.01; A1/A2 genotypes: OR=0.45, P<0.01). CONCLUSION: The polymorphism in DBH gene might play an important role in the susceptibility of Shanghai Chinese Han population to PD.

[A study on the relation between the apolipoprotein E promoter -427C/T polymorphism and Alzheimer's disease].

OBJECTIVE: To determine the relation between the apolipoprotein E(apoE) promoter -427C/T polymorphism and Alzheimer's disease (AD) in a Chinese Han population in Shanghai. METHODS: The apoE promoter -427C/T polymorphism in 104 AD cases and 110 healthy subjects was detected using polymerase chain reaction method and restriction fragment length polymorphism genotyping technique. The differences in polymorphic distribution between the two groups were tested, and odds ratio was computed. RESULTS: No differences in apoE -427C/T genotypic distribution were observed between AD cases and controls (P>0.05). Even after stratification according to apoE epsilon 4 stratum, there was not any polymorphic distribution difference when epsilon 4 carriers or non epsilon 4 carriers were compared with controls (P>0.05). The association between AD and apoE epsilon 4 appeared in the TT group(OR=3.94,95%, CI:22067038, chi-square=21.48, P<0.05), but not in CT or CC group. CONCLUSION: ApoE -427C/T polymorphism was not a susceptibility factor for AD in this Han population in Shanghai.

[Expression variation and mutation analysis of exon 9 and 10 in amyloid precursor protein gene in Alzheimer's disease].

To explore the expression differences of exon 9 and 10 in Amyloid Precursor Protein gene(APP9 approximately 10) in Alzheimer's disease,and detect the probable point mutation appeared in cDNA fragment of APP9 approximately 10 in the Shanghai Han people.semi-quantitative competitive RT-PCR technique was performed to detect the expression of APP9 approximately 10 in peripheral lymphocyte, and the Apolipoprotein E gene(ApoE) and Presenilin 1(PS1)gene were genotyped with PCR-RFLP method. We also analyzed the point mutation in APP9 approximately 10 cDNA through the denatured gel electrophoresis. The results are as follows:1. While compared with healthy controls,expression of APP9 approximately 10 mRNA was significantly enhanced in Alzheimer disease; 2.APOE*epsilon4 allele, the most common genetic risk factor for AD, did not affect the Expression of APP9 approximately 10 mRNA, whereas the APP9 approximately 10 mRNA expression might be increased by the allele 1 of PS1 gene, another probable susceptibility gene of AD.3. No point mutation in APP9 approximately 10 cDNA was detected. In our samples, the expression of APP9 approximately 10 mRNA in AD was significantly different from that of controls, suggesting that the change of peripheral APP9 approximately 10 mRNA expression might be another bio-marker used in clinical diagnosis for AD.