Modulation format identification using the Calinski-Harabasz index.

Modulation format identification (MFI) is a key technology in optical performance monitoring for the next-generation optical network, such as the intelligent cognitive optical network. An MFI scheme based on the Calinski-Harabasz index for a polarization-division multiplexing (PDM) optical fiber communication system is proposed. The numerical simulations were carried out on a 28 Gbaud PDM communication system. The results show that the required minimum optical signal-to-noise ratio values of each modulation format to achieve 100% identification accuracy are all equal to or lower than their corresponding 7% forward error correction thresholds, and the proposed scheme is robust to residual chromatic dispersion. Meanwhile, the proposed scheme was further verified by 20 Gbaud PDM-QPSK/16QAM/32QAM long-haul fiber transmission experiments. The results show that the scheme has a good reliability when fiber non-linear impairments exist. In addition, the complexity of the scheme is significantly lower than that of other clustering-based MFI schemes.

Study Design and Interim Outcomes of Guangzhou Institute of Respiratory Disease COPD Biobank.

BACKGROUND: GIRD COPD Biobank is a multicenter observational study blood-based database with local characteristics, in order to investigate the causes, risk factors, pathogenesis, prevalence patterns and trends of COPD and promote new pathogenic insights in China. METHODS: We enrolled 855 clinically COPD patients and 660 controls with normal lung function. Extensive data collection has been undertaken with questionnaires, clinical measurements, and collection and storage of blood specimens, following Standard Operating Procedures (SOP). All surveys had similar quality controls, supervisions, and training of the investigator team. RESULTS: Since September 2010, a total of 1515 subjects (1116 [73.7%] males; 855 [56.4%] diagnosed with COPD) were enrolled. Analyses of the design and interim results of the GIRD COPD Biobank Study identified patients with COPD were older, lower educational level, a longer history of pack-year smoking, less in kitchen fan usage, X-ray exposure, and history of disease (P < 0.01 for all); Most of the COPD subjects belonged to moderately severe or worse, stratified according to Global Lung Function Initiative (GLI); COPD patients had relatively more co-morbidities than controls; Environmental hazard exposures might be the main contributors to the reported respiratory symptoms; Cold air, haze, and influenza acted the top three factors to induce respiratory symptoms in both COPD cases and controls. CONCLUSION: The GIRD COPD Biobank Study has the potential to provide substantial novel insights into the genetics, biomarkers, environmental and lifestyle aspects of COPD. It is expected to provide new insights for pathogenesis and the long-term progression of COPD.

The Pseudomonas aeruginosa Mannose Sensitive Hamemagglutination Strain (PA-MSHA) Induces a Th1-Polarizing Phenotype by Promoting Human Dendritic Cells Maturation.

Pseudomonas aeruginosa mannose sensitive hamemagglutination strain (PA-MSHA) is a kind of peritrichous P. aeruginosa strain with MSHA fimbriae and has been shown to activate kinds of immunocytes. Dendritic cells (DCs) are specialized antigen-presenting cells required for the stimulating and priming CD4(+) T cells toward the T helper cell type 1 (Th1), Th2 and other different phenotypes. PA-MSHA effecting on Th1 remains an important missing link. Here we demonstrated that PA-MSHA augmented monocytes derived-dendritic cells (Mo-DCs) expression of HLA-DR, co-stimulatory and adhesion molecules, and induced Th1-promoting interleukin-12 and tumor necrosis factor α secretion, in addition, PA-MSHA treated Mo-DCs displayed lesser endocytic capacity. Furthermore, in mixed lymphocyte reactions, allostimulatory capacity of Mo-DCs was enhanced by PA-MSHA, CD4(+) T cells stimulated by PA-MSHA -activated Mo-DCs showed a Th1-polarized cytokine production, increasing secretion of IFN-γ and decreasing secretion of IL-10 and IL-4. Our findings identified PA-MSHA as an important exogenous factor that induced DCs maturation toward a Th1-promoting phenotype.

Peripheral mitochondrial DNA as a neuroinflammatory biomarker for major depressive disorder.

ABSTRACT: In the pathogenesis of major depressive disorder, chronic stress-related neuroinflammation hinders favorable prognosis and antidepressant response. Mitochondrial DNA may be an inflammatory trigger, after its release from stress-induced dysfunctional central nervous system mitochondria into peripheral circulation. This evidence supports the potential use of peripheral mitochondrial DNA as a neuroinflammatory biomarker for the diagnosis and treatment of major depressive disorder. Herein, we critically review the neuroinflammation theory in major depressive disorder, providing compelling evidence that mitochondrial DNA release acts as a critical biological substrate, and that it constitutes the neuroinflammatory disease pathway. After its release, mitochondrial DNA can be carried in the exosomes and transported to extracellular spaces in the central nervous system and peripheral circulation. Detectable exosomes render encaged mitochondrial DNA relatively stable. This mitochondrial DNA in peripheral circulation can thus be directly detected in clinical practice. These characteristics illustrate the potential for mitochondrial DNA to serve as an innovative clinical biomarker and molecular treatment target for major depressive disorder. This review also highlights the future potential value of clinical applications combining mitochondrial DNA with a panel of other biomarkers, to improve diagnostic precision in major depressive disorder.

Does decreased autophagy and dysregulation of LC3A in astrocytes play a role in major depressive disorder?

Astrocytic dysfunction contributes to the molecular pathogenesis of major depressive disorder (MDD). However, the astrocytic subtype that mainly contributes to MDD etiology and whether dysregulated autophagy in astrocytes is associated with MDD remain unknown. Using a single-nucleus RNA sequencing (snRNA-seq) atlas, three astrocyte subtypes were identified in MDD, while C2 State-1Q astrocytes showed aberrant changes in both cell proportion and most differentially expressed genes compared with other subtypes. Moreover, autophagy pathways were commonly inhibited in astrocytes in the prefrontal cortices (PFCs) of patients with MDD, especially in C2 State-1Q astrocytes. Furthermore, by integrating snRNA-seq and bulk transcriptomic data, we found significant reductions in LC3A expression levels in the PFC region of CUMS-induced depressed mice, as well as in postmortem PFC tissues and peripheral blood samples from patients with MDD. These results were further validated by qPCR using whole-blood samples from patients with MDD and healthy controls. Finally, LC3A expression in the whole blood of patients with MDD was negatively associated with the severity of depressive symptoms. Overall, our results underscore autophagy inhibition in PFC astrocytes as a common molecular characteristic in MDD and might reveal a novel potential diagnostic marker LC3A.

Cyanophycin accumulated under nitrogen-fluctuating and high-nitrogen conditions facilitates the persistent dominance and blooms of Raphidiopsis raciborskii in tropical waters.

Nutrient storage is considered a critical strategy for algal species to adapt to a fluctuating nutrient supply. Luxury phosphorus (P) uptake into storage of polyphosphate extends the duration of cyanobacterial dominance and their blooms under P deficiency. However, it is unclear whether nitrogen (N) storage in the form of cyanophycin supports persistent cyanobacterial dominance or blooms in the tropics where N deficiency commonly occurs in summer. In this study, we examined genes for cyanophycin synthesis and degradation in Raphidiopsis raciborskii, a widespread and dominant cyanobacterium in tropical waters; and detected the cyanophycin accumulation under fluctuating N concentrations and its ecological role in the population dynamics of the species. The genes for cyanophycin synthesis (cphA) and degradation (cphB) were highly conserved in 21 out of 23 Raphidiopsis strains. This suggested that the synthesis and degradation of cyanophycin are evolutionarily conserved to support the proliferation of R. raciborskii in N-fluctuating and/or deficient conditions. Isotope 15N-NaNO3 labeling experiments showed that R. raciborskii QDH7 always commenced to synthesize and accumulate cyanophycin under fluctuating N conditions, regardless of whether exogenous N was deficient. When the NO3--N concentration exceeded 1.2 mg L-1, R. raciborskii synthesized cyanophycin primarily through uptake of 15N-NaNO3. However, when the NO3--N concentration was below 1.0 mg L-1, cyanophycin-based N was derived from unlabeled N2, as evidenced by increased dinitrogenase activity. Cells grown under NO3--N < 1.0 mg L-1 had lower cyanophycin accumulation rates than cells grown under NO3--N > 1.2 mg L-1. Our field investigation in a large tropical reservoir underscored the association between cyanophycin content and the population dynamics of R. raciborskii. The cyanophycin content was high in N-sufficient (NO3--N > 0.45 mg L-1) periods, and decreased in N-deficient summer. In summer, R. raciborskii sustained a relatively high biomass and produced few heterocysts (< 1%). These findings indicated that cyanophycin-released N, rather than fixed N, supported persistent R. raciborskii blooms in N-deficient seasons. Our study suggests that the highly adaptive strategy in a N2-fixing cyanobacterial species makes mitigating its bloom more difficult than previously assumed.

[Intraspecific Variation in Growth and Alkaline Phosphatase Activity of Cylindrospermopsis raciborskii Strains in Response to Different Phosphorus Concentrations and Sources].

The cyanobacterial species C. raciborskii are ubiquitous in tropical regions, and its successful invasion into temperate zones has been partially attributed to its ability of survival in low P availability and the existence of multiple ecotypes. To explore the physiological response of different strains to phosphorus fluctuations, four strains of C. raciborskii isolated from the Zhenhai Reservoir were used to investigate their growth and alkaline phosphatase (ALP) activity at different inorganic phosphorus (Pi) concentrations (HP=7.13 mg ·L-1, MP=0.64 mg ·L-1, LP=0.03 mg ·L-1) and different phosphorus forms [dipotassium hydrogen phosphate (K2HPO4), sodium pyrophosphate (K4P2 O7), sodium polyphosphate (K5P3O10), D-glucose-6-phosphate (D-G-6-P), adenosine triphosphate (ATP), cyclic adenosine monophosphate (cAMP)]. Four C. raciborskii strains showed a similar growth response to phosphate changes: their biomass increased with an increase in Pi concentrations, while the ALP activity showed the opposite trend. The ALP activity of C. raciborskii N8 was significantly lower than that of other three strains, regardless of inorganic phosphorus concentrations, suggesting that this strain had a higher adaptability to phosphorus fluctuations. When cultured with different phosphorus forms, the biomass of C. raciborskii N8 and N9 in three dissolved inorganic phosphorus (DIP) compounds were significantly higher than those in three dissolved organic phosphorus (DOP) compounds, with the maximum and minimum specific growth rate in K2HPO4and ATP treatments, respectively. C. raciborskii preferred DIP although they can also utilize DOP to sustain its growth. Under the DOP conditions, the ALP activity of C. raciborskii N8 in the ATP treatment was significantly higher than that in the other two organic phosphorus compounds, while we did not observe similar results in C. raciborskii N9, indicating that strain N8 was more sensitive to DIP deficiency. Our results showed an intraspecific variation within C. raciborskii strains from the same reservoir. Compared with the other strains, strain N8 represented better adaptability to phosphorus fluctuations and DIP deficiency. Variations within C. raciborskii strains may make this species more adaptable to environmental changes and enhance its competitive advantage.

[Effect of ginsenoside Rg2 on chemical myocardial ischemia in rats].

OBJECTIVE: To investigate the protective effect of Ginsenoside Rg2 on Chemical myocardial ischemia. METHOD: The models of myocardial ischemia were built in rats with isoproterenol, sodium nitrite,pituitrin. Ginsenoside Rg2 (iv 2.5, 5.0, 10.0 mg x kg(-1)) were intravenously administered. RESULT: Ginsenoside Rg2 could improve the abnormal electrocardiogram (ECG), reduce the arca of myocardial ischemia and improve the abnormal zymologic value of myocardial. CONCLUSION: Ginsenoside Rg2 has inhibitory function on myocardialischemia.

Genetic variants in MUC4 gene are associated with lung cancer risk in a Chinese population.

Mucin MUC4, which is encoded by the MUC4 gene, plays an important role in epithelial cell proliferation and differentiation. Aberrant MUC4 overexpression is associated with invasive tumor proliferation and poor outcome in epithelial cancers. Collectively, the existing evidence suggests that MUC4 has tumor-promoter functions. In this study, we performed a case-control study of 1,048 incident lung cancer cases and 1,048 age- and sex frequency-matched cancer-free controls in a Chinese population to investigate the role of MUC4 gene polymorphism in lung cancer etiology. We identified nine SNPs that were significantly associated with increased lung cancer risk (P = 0.0425 for rs863582, 0.0333 for rs842226, 0.0294 for rs842225, 0.0010 for rs2550236, 0.0149 for rs2688515, 0.0191 for rs 2641773, 0.0058 for rs3096337, 0.0077 for rs859769, and 0.0059 for rs842461 in an additive model). Consistent with these single-locus analysis results, the haplotype analyses revealed an adverse effect of the haplotype "GGC" of rs3096337, rs859769, and rs842461 on lung cancer. Both the haplotype and diplotype "CTGAGC" of rs863582, rs842226, rs2550236, rs842225, and rs2688515 had an adverse effect on lung cancer, which is also consistent with the single-locus analysis. Moreover, we observed statistically significant interactions for rs863582 and rs842461 in heavy smokers. Our results suggest that MUC4 gene polymorphisms and their interaction with smoking may contribute to lung cancer etiology.