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In this letter, a monolayer graphene-clad microfiber device is designed to achieve ultra-broadband all-optical modulation. Based on the broadband advantage of graphene, we sufficiently discussed the priority absorption characteristic of graphene and continuous wave light saturated absorption characteristic of composite waveguide. Furthermore, superior to previous related publications which the wavelength of pump light is limited, we pioneered and verified that various wavelength light can be used as pump light to achieve all-optical modulation in the designed device. In our experiment, supercontinuum light with spectrum range (0.48 μm−1.7 μm) is modulated by the conventional low-power continuous wave laser diode (808 nm) with pump power under 50 mW. Experimental results for the all-optical modulator achieve modulation depths of ~5.7 dB (1310 nm), ~6.8 dB (1550 nm), and ~7.3 dB (1610 nm), modulation efficiency of ~0.11 dBmW−1 (1310 nm), ~0.14 dBmW−1 (1550 nm), and ~0.15 dBmW−1 (1610 nm), respectively, crossing the O, C, and L bands. The modulation bandwidth reaches 970 nm which is obviously 20 times higher than the modulation bandwidth ~50 nm reported in related publications. This all-optical modulator based on graphene microfiber provides an easy and efficient way to modulate the ultra-broadband light with very low pump power. [ABSTRACT FROM AUTHOR]

Disturbances in GABAergic system have been observed in schizophrenics.1,2,3 In the present study, population association analysis was performed on 19 SNPs in the a1, ß2, ?2, ? and p subunit genes of GABAA receptor. Five SNPs in GABRB2, namely B2I7G1584T, rs1816071, rs194072, rs252944 and rs187269, were found to be significantly associated, and their haplotypes in linkage disequilibrium, with schizophrenia. This represents the first report on any disease association of SNPs in the human GABAA receptor genes, and focuses attention on the GABAergic hypothesis of schizophrenia etiology.3,4Molecular Psychiatry (2004) 9, 603-608. doi:10.1038/sj.mp.4001461 Published online 16 December 2003 [ABSTRACT FROM AUTHOR]

Presents a letter to the editor about research on apolipoprotein E allele in relation to late-onset Alzheimer's disease.

Objective: This study explored the preoperative prognostic factors of patients with glioblastoma multiforme (GBM) in order to propose a preoperative prognosis estimation model. Methods: The clinical data of 416 patients diagnosed with GBM in Beijing Tiantan Hospital affiliated to Capital Medical University from 2008 to 2015 were retrospectively reviewed.A total of nine factors: gender, age, duration of symptoms, preoperative epilepsy, preoperative muscle weakness, preoperative headache, preoperative KPS score, tumor location and tumor diameter were enrolled in the survival analysis.The significant factors identified by Kaplan-Meier plot were further collected in the multivariate Cox regression analysis.On the basis of multivariate analysis results, a preoperative prognosis estimation model was founded. Results: Univariate analysis showed that Age ≥50 years, without preoperative epilepsy, tumor located in non-frontotemporal lobe, tumor diameter ≥6 cm and preoperative KPS score <70 were prognostic risk factors ( P <0.05). Multivariate analysis revealed that Age ≥50 years, without preoperative epilepsy, tumor located in non-frontotemporal lobe were independent risk factors ( P <0.05). The prognostic estimation model based on the independent risk factors divided the whole cohort into three subgroups with different survival ( P <0.001). Conclusions: The more risk factors, the higher score but poorer prognosis. Patients in the high-risk group had lower gross total resection degree but higher rate of postoperative complications, which suggested that aggressive resection was not suitable for high-risk patients.

We evaluated association of polymorphisms in the CTLA-4 gene with the risk of type 1 diabetes mellitus. Comprehensive meta-analysis was applied to case-control studies of the association between CTLA-4 and type 1 diabetes mellitus to assess the joint evidence for the association, the influence of individual studies, and evidence for publication bias. We searched PubMed, Medline, Embase, Cochrane Library, and reference lists of relevant studies to February 2012, and made email contact with authors. For the case-control studies, we found 1) support for an association between CTLA-4 and type 1 diabetes mellitus, 2) no evidence that this association was accounted for by any one study, and 3) no evidence for publication bias. In all, although the association between CTLA-4 polymorphisms and type 1 diabetes mellitus is weak, we suggest that it is real. Further studies are needed to clarify what variant of CTLA-4 (or some related gene) accounts for this association.

Exposure to prenatal undernutrition or malnutrition increases the risk of schizophrenia, although little is known about the mechanism. Pro-inflammatory factors are critical in brain development, and are believed to play an important role in neurodevelopmental disorders associated with prenatal exposure to infection, including schizophrenia. However it is not known whether pro-inflammatory factors also mediate the effects on the fetus of prenatal malnutrition or undernutrition. In this study, we established a new prenatal undernourished rat model induced by maternal exposure to a diet restricted to 50% of the low (6%) protein diet (RLP50). We observed the disappearance of maternal nest-building behavior in the RLP50 dams, increased levels of TNFA and IL6 in the placentas (P<0.001; P=0.879, respectively) and fetal livers (P<0.001; P<0.05, respectively), and a decrease in the fetal brains (P<0.05; P<0.01, respectively). Our results are similar to previous studies of maternal infection, which implies that a common pathway mediated by pro-inflammatory factors may contribute to the brain development, consequently increasing the risk of schizophrenia and other psychiatric diseases programmed by varied maternal adversities. We also provide a new prenatal undernourished model for researching prenatal problems, which differs from previous malnourished model in terms of the maternal behavior of dams and of observed pro-inflammatory factor levels in fetal tissues.

The interleukin-10 (IL-10) gene has been identified as a susceptibility gene for schizophrenia in Caucasians. A previous case-control study conducted by our group revealed a weak association between polymorphism, -592C/A, of the IL-10 gene promoter and schizophrenia. Our present study was aimed at confirming the association of the IL-10 promoter with schizophrenia using 197 Han Chinese sib-pair families. A family-based association test (FBAT) and haplotype analysis was undertaken using the FBAT v1.5.5. The global TDT was significant for a different polymorphism, -1082G/A (chi2=13.16, P=0.000285) and that the allele -1082G was preferentially transmitted to schizophrenia-affected children. Furthermore, haplotype TDT analysis showed that haplotype "GCC" was significantly associated with the disease (chi2=8.1, P=0.00443). Our results also indicate that the IL-10 gene may play a significant role in the etiology of schizophrenia among Han Chinese.

Neurotransmitter-based hypotheses have so far led to only moderate success in predicting new pathogenetic findings in etiology of schizophrenia. On the other hand, the more recent oligodendroglia hypotheses of this disorder have been supported by an increasing body of evidence. For example, the expression level of the myelin associated glycoprotein (MAG) gene has been shown to be significantly lower in schizophrenia patient groups compared to control groups. Such an effect might be a result of genetic variations of the MAG gene. In order to test this hypothesis, we genotyped four markers within the MAG locus in 413 trios sample of the Han Chinese using allele-specific PCR. None of the four markers revealed noticeable allelic significance. However, the four-marker and two-marker haplotypes covering components rs720309 and rs720308 were observed to be significantly associated with schizophrenia (P < 0.0001) in this study. In addition, we identified one common risk haplotype TA (rs720309-rs720308, present in 78.5% of the general population) that showed increased evidence of overtransmission from parents to affected offspring (P = 0.0001). The results demonstrated MAG might play a role in genetic susceptibility to schizophrenia. Furthermore, our finding of a possible association between the MAG locus and schizophrenia is in agreement with the hypotheses of oligodendrltic and myelination dysfunction.

Polymorphisms at positions -491, -427 and -219 in the promoter region of the Apolipoprotein E APOE gene have been variously reported to confer an increased risk of developing Alzheimer's disease (AD) independent of the effect of epsilon 2, 3 or 4 alleles in exon 4. In order to assess APOE promoter polymorphisms as independent risk factors in AD we have compared results in 183 definite or probable AD cases with 133 controls. We assayed markers at sites -491, -427, -219, and +113 in APOE gene and a polymorphic Hha1 site in the nearby APOC1 gene. We found that APOE promoter polymorphisms and APOC1 insertion alleles were significantly associated with AD. However, after stratification for epsilon 4 allele, only the A allele at -491 in APOE remained significantly associated with AD. The effects of the other markers depended almost entirely upon linkage disequilibrium with epsilon 4 allele, and only trends remained when cases and controls were stratified for the presence or absence of epsilon 4 allele. This occurred irrespective of whether markers were examined separately or together as haplotypes. So in the Chinese population only APOE -491 promoter alleles confer significant risk of AD independent of epsilon 4 status.

Several pieces of evidence implicate serotonin receptors in the aetiology of schizophrenia, and recently a number of studies have reported a genetic association between the 102T/C polymorphism of serotonin receptor type 2A gene and schizophrenia. Unfortunately a number of failures to replicate these positive associations in both Caucasian and Chinese populations have also been reported. We have examined the 102T/C polymorphism by PCR amplification and restriction analysis of DNA from: 202 schizophrenics and 202 controls from Shanghai; 112 schizophrenics and 224 parents from Chengdu, Cina; and 253 schizophrenics and 244 controls from the the UK. We find no evidence of association or transmission disequilibrium between the 102T/C polymorphism and schizophrenia in any of the groups we have examined. We conclude that either the original positive reports occurred by chance or any effect must be minimal, and urge caution in interpreting small positive results derived using data from different centres.