Aiming for a new and more comprehensive DIB catalog between 4,000 and 9,000Å, we revisited the Atlas Catalog based on the observations of HD 183143 and HD 204827 (Hobbs et al. 2008 and). Twenty-five medium-to-highly reddened sight lines were selected, sampling a variety of spectral types of the background star and the interstellar environments. The median SNR of these spectra is ~ 1,300 around 6,400Å. Compared to the Atlas Catalog, 22 new DIBs were found, and the boundaries of 27 (sets) of DIBs were adjusted, resulting in an updated catalog containing 559 DIBs that we refer to as the Apache Point Observatory Catalog of Optical Diffuse Interstellar Bands. Measurements were then made based on this catalog. We found our survey most sensitive between 5,500 and 7,000Å due largely to the local SNR of the spectra, the relative absence of interfering stellar lines, and the weakness of telluric residuals. For our data sample, the number of DIBs detected in a given sight line is mostly dependent on E B-V and less on the spectral type of the background star. Some dependence on f H2 is observed, but less well-determined due to the limited size of the data sample. The variations of the wavelengths of each DIB in different sight lines are generally larger than those of the known interstellar lines CH + , CH, and K I.Those variations could be due to the inherent error in the measurement, or to differences in the velocity components among sight lines.

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Abstract:We study the behavior of eight diffuse interstellar bands (DIBs) in different interstellar environments, as characterized by the fraction of hydrogen in molecular form (f H2 ), with comparisons to the corresponding behavior of various known atomic and molecular species. The equivalent widths of the five "normal" DIBs (ll5780.5, 5797.1, 6196.0, 6283.8, and 6613.6), normalized to E B-V , show a "Lambda-shaped" behavior: they increase at low f H2 , peak at f H2 ~ 0.3, and then decrease. The similarly normalized column densities of Ca, Ca + , Ti + , and CH + also decline for f H2 > 0.3. In contrast, the normalized column densities of Na, K, CH, CN, and CO increase monotonically with f H2 , and the trends exhibited by the three C 2 DIBs (ll4726.8, 4963.9, and 4984.8) lie between those two general behaviors. These trends with f H2 are accompanied by cosmic scatter, the dispersion at any given f H2 being significantly larger than the individual errors of measurement. The Lambda-shaped trends suggest the balance between creation and destruction of the DIB carriers differs dramatically between diffuse atomic and diffuse molecular clouds; additional processes besides ionization and shielding are needed to explain those observed trends. Except for several special cases, the highest W l (5780)/W l (5797) ratios, characterizing the so-called "sigma-zeta effect", occur only at f H2 < 0.2. We propose a sequence of DIBs based on trends in their pair-wise strength ratios with increasing f H2 . In order of increasing environmental density, we find the l6283.8 and l5780.5 DIBs, the l6196.0 DIB, the l6613.6 DIB, the l5797.1 DIB, and the C 2 DIBs.

BackgroundHormones and immune imbalance are critical factors in polycystic ovary syndrome (PCOS). The alternation of immune microenvironment of oocytes may play a significant role in infertility of PCOS patients.ObjectiveThis study explores the role of follicular fluid microenvironment change in inflammatory pathways activation of granulosa cells (GCs) in PCOS women infertility.MethodsWe enrolled 27 PCOS patients and 30 controls aged 22 to 38 years who underwent IVF and collected their luteinized granulosa cells (LGCs). Meanwhile, a granulosa-like tumor cell line (KGN) as a cell-model assisted this study. Key inflammatory markers in human ovarian GCs and follicular fluid were detected by RT-qPCR, Western blotting, or ELISA. The KGN cells were treated with follicle supernatant mixed with normal medium to simulate the microenvironment of GCs in PCOS patients, and the inflammation indicators were observed. The assembly of NLRP3 inflammasomes was detected by immunofluorescence techniques. Dihydroethidium assay and EdU proliferation assay were used to detect ROS and cell proliferation by flow cytometry.ResultsCompared with normal controls (n = 19), IL-1β (P = 0.0005) and IL-18 (P = 0.021) in the follicular fluid of PCOS patients (n = 20) were significantly increased. The NF-κB pathway was activated, and NLRP3 inflammasome was formatted in ovarian GCs of PCOS patients. We also found that inflammation of KGN cells was activated with LPS irritation or stimulated by follicular fluid from PCOS patients. Finally, we found that intracellular inflammation process damaged mitochondrial structure and function, which induced oxidative stress, affected cellular metabolism, and impaired cell proliferation.ConclusionInflammatory microenvironment alteration in the follicular fluid of PCOS patients leads to activated inflammatory pathway in GCs, serving as a crucial factor that causes adverse symptoms in patients. This study provides a novel mechanism in the inflammatory process of PCOS.

Mitochondria serve as an energy plant and participate in a variety of signaling pathways to regulate cellular metabolism, survival and immunity. Mitochondrial dysfunction, in particular in cardiomyocytes, is associated with the development and progression of cardiovascular disease, resulting in heart failure, cardiomyopathy, and cardiac ischemia/reperfusion injury. Therefore, mitochondrial quality control processes, including post-translational modifications of mitochondrial proteins, mitochondrial dynamics, mitophagy, and formation of mitochondrial-driven vesicles, play a critical role in maintenance of mitochondrial and even cellular homeostasis in physiological or pathological conditions. Accumulating evidence suggests that mitochondrial quality control in cardiomyocytes is able to improve cardiac function, rescue dying cardiomyocytes, and prevent the deterioration of cardiovascular disease upon external environmental stress. In this review, we discuss recent progress in understanding mitochondrial quality control in cardiomyocytes. We also evaluate potential targets to prevent or treat cardiovascular diseases, and highlight future research directions which will help uncover additional mechanisms underlying mitochondrial homeostasis in cardiomyocytes.

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The mitochondrion, the ATP-producing center, is both physically and functionally associated with almost all other organelles in the cell. Mitochondrial-associated membranes (MAMs) are involved in a variety of biological processes, such as lipid exchange, protein transport, mitochondrial fission, mitophagy, and inflammation. Several inflammation-related diseases in the cardiovascular system involve several intracellular events including mitochondrial dysfunction as well as disruption of MAMs. Therefore, an in-depth exploration of the function of MAMs will be of great significance for us to understand the initiation, progression, and clinical complications of cardiovascular disease (CVD). In this review, we summarize the recent advances in our knowledge of MAM regulation and function in CVD-related cells. We discuss the potential roles of MAMs in activating inflammation to influence the development of CVD.