Reconstruction of Velocity Curve in Long Stroke and High Dynamic Range Laser Interferometry.

To study the law that governs the complex movements of the mechanism in the process of automatic weapon operation, the velocity tracking test technology of photon Doppler velocimetry is introduced to accurately measure velocity, displacement and acceleration, on the condition that there are long displacement and rapid velocity change. In the traditional way, out of interference signal time-frequency (TF) transformation draws TF distribution, and then by modulus maxima frequency extraction, comes to the law of velocity change. Due to the influence resulting from the change of fundamental signal as well as that of light intensity signal in the test, based on the TF distribution obtained by TF transformation, the traditional modulus maxima frequency extraction can extract frequency signals, but they show abnormal sudden changes at some moments, making the velocity discontinuous, unsmooth and unreal, which brings obvious errors to the subsequent calculation of acceleration and accurate displacement. Addressing the above-mentioned problems, this paper proposes a ridge extracting correction algorithm based on modulus maxima frequency extraction; this method, based on a large number of experiments where rodless cylinders are used to simulate the motion of a gun automatic mechanism, conducts a detailed calculation and analysis of the experimental results. A comparison of the two algorithms' processing results, in terms of the speed, displacement and acceleration, suggests that the ridge extracting correction algorithm successfully corrects the frequency selection error, which draws a more continuous and, therefore, effective curve of the velocity change, and by so doing, the error of the displacement test (within 1.36 m displacement) is reduced from more than 3.6% to less than 0.58%, and the uncertainty dropped 97.07%. All these show that the accurate measurement of velocity, displacement and acceleration, with sudden and rapid velocity changes considered, is realized successfully.

Lack of association of FcγRIIIb polymorphisms with systemic lupus erythematosus: a meta-analysis.

Systemic lupus erythematosus (SLE) is a complex autoimmune disease. Fcγ receptor genes have been suggested to play an important role in the pathogenesis of SLE and lupus nephritis (LN). This study aims to assess the association between FcγRIIIb-NA1/NA2 polymorphism and the susceptibility to SLE and lupus nephritis. Relevant studies were identified from electronic databases. A meta-analysis was performed for heterogeneity test and pooled OR calculation. The overall OR of NA2/NA2 homozygous genotype and NA2 allele frequency showed no significant association with SLE and lupus nephritis. Similarly, the association between FcγRIIIb-NA1/NA2 polymorphism and SLE and lupus nephritis was not found in European and Asian population. Taken together, our results suggest that FcγRIIIb might not be a susceptibility gene for SLE and lupus nephritis.

Gender and age influence on clinical and laboratory features in Chinese patients with systemic lupus erythematosus: 1,790 cases.

This study aims to review the cumulative clinical and laboratory data of 1,790 Chinese patients with systemic lupus erythematosus. Data were compared separately between male and female patients for each disease onset age groups and among three disease onset age groups in male and female patients. The ratio of female to male was 9.2:1, with differences among three age groups. There was no difference in mean age at onset between females and males. But diagnosis delay in male patients is shorter than in females. When compared with females, in adult-onset patients, males presented more frequently with serositis, pleuritis and discoid rash, but less frequently with malar rash, alopecia, oral ulcers, elevated erythrocyte sedimentation rate, anti-nuclear, anti-SSA and anti-SSB antibodies. In younger-onset group, males have less discoid rash. In older-onset group, males have less anti-SSA antibodies. In male patients, only anti-SSB antibodies were different in three age groups and negatively correlate to age. Among female patients, age had negative correlations with malar rash, discoid rash, photosensitivity, anti-dsDNA, anti-Sm, anti-SSB and anti-rRNP antibodies, but positive correlation with leucopenia. We conclude that women of childbearing age possess a distinct clinical and laboratory profile. In addition, differences in disease manifestations seem to be correlated with female sex hormones rather than age.

A meta-analysis of the association of STAT4 polymorphism with systemic lupus erythematosus.

STAT4 has been newly identified as a susceptibility gene for systemic lupus erythematosus (SLE) in recent reports. To more precisely estimate the association between STAT4 polymorphism and SLE risk, a meta-analysis was performed. Studies on the association of STAT4 rs7574865 or rs7601754 with SLE were fully considered and carefully selected using three electronic databases (PubMed, Embase, and Web of Science). A total of 17 comparisons from 8 relevant studies involving 7,381 patients and 11,431 controls were included to analyze the association between STAT4 rs7574865 and SLE risk. The pooled OR for the minor T allele of STAT4 rs7574865 was 1.65 (95% CI 1.56-1.75, P < 0.001) in SLE. In a subgroup analysis by ethnicity, the degree of risk of STAT4 rs7574865 with SLE susceptibility was similar in populations of European or Asian origin, although significant differences in the minor T allele frequencies were observed in the two population controls. As for rs7601754, there were five comparisons from four relevant studies involving 2,498 patients and 4,825 controls in this meta-analysis. The pooled OR for the minor C allele of STAT4 rs7601754 was 0.67 (95% CI 0.59-0.75, P < 0.001) in SLE. Conversely, the major T allele of STAT4 rs7601754 might be a risk factor for SLE risk. In conclusion, our results do support STAT4 rs7574865 polymorphism as a susceptibility factor for SLE in populations of European and Asian origin. Our results also suggest that STAT4 rs7601754 polymorphism might be associated with SLE risk.

Meta analysis on the association between FcgammaRIIa-R/H131 polymorphisms and systemic lupus erythematosus.

In order to study the association between FcgammaRIIa gene polymorphisms and the risk of systemic lupus erythematosus (SLE) and lupus nephritis, relevant studies were identified from electronic databases. A meta-analysis of relevant studies was performed for heterogeneity test and pooled OR calculation. When all groups were pooled, a significant association of FcgammaRIIa-R131 allele and increased SLE risk was found. But this association was not observed in lupus nephritis. In the subgroup analysis, a clear effect of R allele in SLE was shown in European and Asian subgroups. Similarly, RR homozygous genotype was found to be a risk factor of SLE and lupus nephritis. The association between RR genotype and SLE was shown in European and Asian descents. However, the association between RR genotype and lupus nephritis was not found in any ethnic subgroups. Taken together, our study suggests that the FcgammaRIIa-R/H131 polymorphism might contribute to the susceptibility to SLE and lupus nephritis.

Maternally inherited aminoglycoside-induced and nonsyndromic hearing loss is associated with the 12S rRNA C1494T mutation in three Han Chinese pedigrees.

We report here the clinical, genetic and molecular characterization of three Han Chinese pedigrees with maternally transmitted aminoglycoside-induced and nonsyndromic bilateral hearing loss. Clinical evaluation revealed the wide range of severity, age-at-onset and audiometric configuration of hearing impairment in matrilineal relatives in these families. The penetrances of hearing loss in these pedigrees were 28%, 20%, and 15%, with an average of 21%, when aminoglycoside-induced deafness was included. When the effect of aminoglycosides was excluded, the penetrances of hearing loss in these seven pedigrees were 21%, 13% and 8%, with an average of 14%. Sequence analysis of the complete mitochondrial genomes in these pedigrees showed the presence of the deafness-associated 12S rRNA C1494T mutation, in addition to distinct sets of mtDNA polymorphism belonging to Eastern Asian haplogroups F1a1, F1a1 and D5a2, respectively. This suggested that the C1494T mutation occurred sporadically and multiplied through evolution of the mtDNA. The absence of functionally significant mutations in tRNA and rRNAs or secondary LHON mutations in their mtDNA suggests that these mtDNA haplogroup-specific variants may not play an important role in the phenotypic expression of the C1494T mutation in those Chinese families. In addition, the lack of significant mutation in the GJB2 gene ruled out the possible involvement of GJB2 in the phenotypic expression of the C1494T mutation in those affected subjects. However, aminoglycosides and other nuclear modifier genes play a modifying role in the phenotypic manifestation of the C1494T mutation in these Chinese families.

Very low penetrance of hearing loss in seven Han Chinese pedigrees carrying the deafness-associated 12S rRNA A1555G mutation.

Mutations in mitochondrial DNA (mtDNA) have been found to be associated with sensorineural hearing loss. We report here the clinical, genetic and molecular characterizations of seven Han Chinese pedigrees with aminoglycoside-induced and nonsyndromic bilateral hearing loss. Clinical evaluation revealed the variable phenotype of hearing impairment including severity, age-at-onset and audiometric configuration in these subjects. The penetrance of hearing loss in these pedigrees ranged from 3% to 29%, with an average of 13.6%, when aminoglycoside-induced deafness was included. When the effect of aminoglycosides was excluded, the penetrances of hearing loss in these seven pedigrees varied from 0% to 17%, with an average of 5.3%. Sequence analysis of the complete mitochondrial genomes in these pedigrees showed the presence of the deafness-associated 12S rRNA A1555G mutation, in addition to distinct sets of mtDNA polymorphism belonging to East Asian haplogroups B4, D4, D5 and F1, respectively. This suggested that the A1555G mutation occurred sporadically and multiplied through evolution of the mtDNA in China. Despite the presence of several evolutionary conservative variants in protein-encoding genes, there was the absence of functionally significant mutations in tRNA and rRNAs or secondary LHON mutations in these seven Chinese families. These suggest that these mtDNA haplogroup-specific variants may not play an important role in the phenotypic expression of the A1555G mutation in those Chinese families with very low penetrance of hearing loss. However, aminoglycosides appear to be a major modifier factor for the phenotypic manifestation of the A1555G mutation in these Chinese families.