The case of NGC 6302: the impact of shocks in the derivation of nitrogen abundances

ABSTRACT High nitrogen abundance is characteristic of Type I planetary nebulae, as well as their highly filamentary structure. In the present work, we test the hypothesis of shocks as a relevant excitation mechanism for a Type I nebula, NGC 6302, using recently released diagnostic diagrams to distinguish shocks from photoexcitation. The construction of the diagrams depends on emission-line ratios and kinematical information. NGC 6302 shows the relevance of shocks in peripheral regions and their importance to the whole nebula. Using shocks, we question the usual assumption of ionization correction factor calculation, justifying a warning regarding broadly used abundance derivation methods. From kinematical analysis, we derive a new distance for NGC 6302 of $805\pm 143\,$ pc.

Download Full-text

IFU Spectroscopy of Southern Planetary Nebulae V: Low-Ionisation Structures

Publications of the Astronomical Society of Australia ◽

10.1017/pasa.2017.30 ◽

2017 ◽

Vol 34 ◽

Cited By ~ 8

Author(s):

A. Ali ◽

M. A. Dopita

Keyword(s):

Emission Line ◽

Planetary Nebulae ◽

Central Star ◽

Chemical Compositions ◽

Physical Analysis ◽

Type I ◽

High Excitation ◽

Chemical Abundances ◽

Physical Conditions ◽

Integral Field Spectroscopy

AbstractIn this fifth paper of the series, we examine the spectroscopy and morphology of four southern Galactic planetary nebulae Hen 2-141, NGC 5307, IC 2553, and PB 6 using new integral field spectroscopy data. The morphologies and ionisation structures of the sample are given as a set of emission-line maps. In addition, the physical conditions, chemical compositions, and kinematical characteristics of these objects are derived. The results show that PB 6 and Hen 2-141 are of very high excitation classes and IC 2553 and NGC 5307 are mid to high excitation objects. The elemental abundances reveal that PB 6 is of Type I, Hen 2-141 and IC 2553 are of Type IIa, and NGC 5307 is of Type IIb/III. The observations unveil the presence of well-defined low-ionisation structures or ‘knots’ in all objects. The diagnostic diagrams reveal that the excitation mechanism of these knots is probably by photoionisation of dense material by the nebular central stars. The physical analysis of six of these knots show no significant differences with their surrounding nebular gas, except their lower electron densities. In spite of the enhancement of the low-ionisation emission lines of these knots, their chemical abundances are nearly comparable to their surrounding nebulae, with the exception of perhaps slightly higher nitrogen abundances in the NGC 5307 knots. The integrated spectrum of IC 2553 reveals that nearly all key lines that have led researchers to characterise its central star as a weak-emission line star type are in fact of nebular origin.

Download Full-text

The Weak Emission Line Stars

Symposium - International Astronomical Union ◽

10.1017/s0074180900208589 ◽

2003 ◽

Vol 209 ◽

pp. 235-236

Author(s):

Jeffrey Fogel ◽

Orsola De Marco ◽

George Jacoby

Keyword(s):

Emission Line ◽

Absorption Line ◽

Planetary Nebula ◽

Planetary Nebulae ◽

Emission Lines ◽

Type I ◽

Evolutionary Sequence ◽

Lower Mass ◽

Stellar Temperatures ◽

Central Stars

In this paper, we study the evolution of the weak emission line central stars of planetary nebula (WELS), which are similar to the H-deficient Wolf-Rayet central stars except for systematically weaker emission lines. Our attempts at finding an evolutionary sequence for the WELS similar to what was established for Wolf-Rayet central stars, were unsuccessful. No correlation was found between any of the analysed quantities: emission and absorption line fluxes or stellar and nebular parameters from the literature. It does appear, however, that WELS have intermediate stellar temperatures (30–80 kK), and do not reside in the middle of Type I planetary nebulae, possibly indicating lower mass precursors.

Download Full-text

STING and cGAS gene expressions were downregulated among HIV-1-infected persons after antiretroviral therapy

Virology Journal ◽

10.1186/s12985-021-01548-6 ◽

2021 ◽

Vol 18 (1) ◽

Author(s):

Lorena Leticia Peixoto de Lima ◽

Allysson Quintino Tenório de Oliveira ◽

Tuane Carolina Ferreira Moura ◽

Ednelza da Silva Graça Amoras ◽

Sandra Souza Lima ◽

...

Keyword(s):

Gene Expression ◽

Viral Load ◽

T Cell ◽

Antiretroviral Therapy ◽

Cell Count ◽

Enzyme Linked Immunosorbent Assay ◽

Type I ◽

Α Level ◽

The Impact ◽

Hiv 1

Abstract Background The HIV-1 epidemic is still considered a global public health problem, but great advances have been made in fighting it by antiretroviral therapy (ART). ART has a considerable impact on viral replication and host immunity. The production of type I interferon (IFN) is key to the innate immune response to viral infections. The STING and cGAS proteins have proven roles in the antiviral cascade. The present study aimed to evaluate the impact of ART on innate immunity, which was represented by STING and cGAS gene expression and plasma IFN-α level. Methods This cohort study evaluated a group of 33 individuals who were initially naïve to therapy and who were treated at a reference center and reassessed 12 months after starting ART. Gene expression levels and viral load were evaluated by real-time PCR, CD4+ and CD8+ T lymphocyte counts by flow cytometry, and IFN-α level by enzyme-linked immunosorbent assay. Results From before to after ART, the CD4+ T cell count and the CD4+/CD8+ ratio significantly increased (p < 0.0001), the CD8+ T cell count slightly decreased, and viral load decreased to undetectable levels in most of the group (84.85%). The expression of STING and cGAS significantly decreased (p = 0.0034 and p = 0.0001, respectively) after the use of ART, but IFN-α did not (p = 0.1558). Among the markers evaluated, the only markers that showed a correlation with each other were STING and CD4+ T at the time of the first collection. Conclusions ART provided immune recovery and viral suppression to the studied group and indirectly downregulated the STING and cGAS genes. In contrast, ART did not influence IFN-α. The expression of STING and cGAS was not correlated with the plasma level of IFN-α, which suggests that there is another pathway regulating this cytokine in addition to the STING–cGAS pathway.

Download Full-text

The Dynamic Interaction between Extracellular Matrix Remodeling and Breast Tumor Progression

Cells ◽

10.3390/cells10051046 ◽

2021 ◽

Vol 10 (5) ◽

pp. 1046

Author(s):

Jorge Martinez ◽

Patricio C. Smith

Keyword(s):

Extracellular Matrix ◽

Type I Collagen ◽

Cell Metabolism ◽

Breast Tumors ◽

Extracellular Matrix Remodeling ◽

Type I ◽

Matrix Remodeling ◽

Desmoplastic Reaction ◽

The Impact

Desmoplastic tumors correspond to a unique tissue structure characterized by the abnormal deposition of extracellular matrix. Breast tumors are a typical example of this type of lesion, a property that allows its palpation and early detection. Fibrillar type I collagen is a major component of tumor desmoplasia and its accumulation is causally linked to tumor cell survival and metastasis. For many years, the desmoplastic phenomenon was considered to be a reaction and response of the host tissue against tumor cells and, accordingly, designated as “desmoplastic reaction”. This notion has been challenged in the last decades when desmoplastic tissue was detected in breast tissue in the absence of tumor. This finding suggests that desmoplasia is a preexisting condition that stimulates the development of a malignant phenotype. With this perspective, in the present review, we analyze the role of extracellular matrix remodeling in the development of the desmoplastic response. Importantly, during the discussion, we also analyze the impact of obesity and cell metabolism as critical drivers of tissue remodeling during the development of desmoplasia. New knowledge derived from the dynamic remodeling of the extracellular matrix may lead to novel targets of interest for early diagnosis or therapy in the context of breast tumors.

Download Full-text

Treadmill Running Changes Endothelial Lipase Expression: Insights from Gene and Protein Analysis in Various Striated Muscle Tissues and Serum

Biomolecules ◽

10.3390/biom11060906 ◽

2021 ◽

Vol 11 (6) ◽

pp. 906

Author(s):

Agnieszka Mikłosz ◽

Bartłomiej Łukaszuk ◽

Adrian Chabowski ◽

Jan Górski

Keyword(s):

Protein Expression ◽

Density Lipoprotein ◽

Treadmill Running ◽

Endothelial Lipase ◽

Type I ◽

Fiber Types ◽

Gene And Protein Expression ◽

Single Bout ◽

The Impact ◽

White Gastrocnemius

Endothelial lipase (EL) is an enzyme capable of HDL phospholipids hydrolysis. Its action leads to a reduction in the serum high-density lipoprotein concentration, and thus, it exerts a pro-atherogenic effect. This study examines the impact of a single bout exercise on the gene and protein expression of the EL in skeletal muscles composed of different fiber types (the soleus—mainly type I, the red gastrocnemius—mostly IIA, and the white gastrocnemius—predominantly IIX fibers), as well as the diaphragm, and the heart. Wistar rats were subjected to a treadmill run: 1) t = 30 [min], V = 18 [m/min]; 2) t = 30 [min], V = 28 [m/min]; 3) t = 120 [min], V = 18 [m/min] (designated: M30, F30, and M120, respectively). We established EL expression in the total muscle homogenates in sedentary animals. Resting values could be ordered with the decreasing EL protein expression as follows: endothelium of left ventricle > diaphragm > red gastrocnemius > right ventricle > soleus > white gastrocnemius. Furthermore, we observed that even a single bout of exercise was capable of inducing changes in the mRNA and protein level of EL, with a clearer pattern observed for the former. After 30 min of running at either exercise intensity, the expression of EL transcript in all the cardiovascular components of muscles tested, except the soleus, was reduced in comparison to the respective sedentary control. The protein content of EL varied with the intensity and/or duration of the run in the studied whole tissue homogenates. The observed differences between EL expression in vascular beds of muscles may indicate the muscle-specific role of the lipase.

Download Full-text

Extrusion Processing of Pure Chokeberry (Aronia melanocarpa) Pomace: Impact on Dietary Fiber Profile and Bioactive Compounds

Foods ◽

10.3390/foods10030518 ◽

2021 ◽

Vol 10 (3) ◽

pp. 518

Author(s):

Vera Schmid ◽

Jan Steck ◽

Esther Mayer-Miebach ◽

Diana Behsnilian ◽

Mirko Bunzel ◽

...

Keyword(s):

Dietary Fiber ◽

Water Solubility ◽

Partial Substitution ◽

Type I ◽

Food Ingredient ◽

Pectic Polysaccharides ◽

Thermomechanical Stress ◽

Extrusion Processing ◽

Aronia Melanocarpa ◽

The Impact

The partial substitution of starch with dietary fiber (DF) in extruded ready-to-eat texturized (RTE) cereals has been suggested as a strategy to reduce the high glycemic index of these food products. Here, we study the impact of extrusion processing on pure chokeberry (Aronia melanocarpa) pomace powder (CPP) rich in DF and polyphenols (PP) focusing on the content and profile of the DF fractions, stability of PP, and techno-functional properties of the extrudates. Using a co-rotating twin-screw extruder, different screw speeds were applied to CPP with different water contents (cw), which resulted in specific mechanical energies (SME) in the range of 145–222 Whkg−1 and material temperatures (TM) in the range of 123–155 °C. High molecular weight soluble DF contents slightly increase with increasing thermomechanical stress up to 16.1 ± 0.8 g/100 g dm as compared to CPP (11.5 ± 1.2 g/100 g dm), but total DF (TDF) contents (58.6 ± 0.8 g/100 g dm) did not change. DF structural analysis revealed extrusion-based changes in the portions of pectic polysaccharides (type I rhamnogalacturonan) in the soluble and insoluble DF fractions. Contents of thermolabile anthocyanins decrease linearly with SME and temperature from 1.80 ± 0.09 g/100 g dm in CPP to 0.24 ± 0.06 g/100 g dm (222 Whkg−1, 155 °C), but phenolic acids and flavonoids appear to be largely unaffected. Resulting techno-functional (water absorption and water solubility) and physical properties related to the sensory characteristics (expansion, hardness, and color) of pure CPP extrudates support the expectation that granulated CPP extrudates may be a suitable food ingredient rich in DF and PP.

Download Full-text

Trabecular Bone is Increased in a Rat Model of Polycystic Ovary Syndrome

Experimental and Clinical Endocrinology & Diabetes ◽

10.1055/a-1284-5491 ◽

2020 ◽

Author(s):

Lady Katerine Serrano Mujica ◽

Werner Giehl Glanzner ◽

Amanda Luiza Prante ◽

Vitor Braga Rissi ◽

Gabrielle Rebeca Everling Correa ◽

...

Keyword(s):

Polycystic Ovary Syndrome ◽

Bone Formation ◽

Type I Collagen ◽

Polycystic Ovary ◽

Osteoclast Differentiation ◽

Bone Volume ◽

Negative Regulator ◽

Type I ◽

Ovary Syndrome ◽

The Impact

AbstractPolycystic ovary syndrome (PCOS) in an intricate disorder characterized by reproductive and metabolic abnormalities that may affect bone quality and strength along with the lifespan. The present study analysed the impact of postnatal androgenization (of a single dose of testosterone propionate 1.25 mg subcutaneously at day 5 of life) on bone development and markers of bone metabolism in adult female Wistar rats. Compared with healthy controls, the results of measurements of micro-computed tomography (microCT) of the distal femur of androgenized rats indicated an increased cortical bone volume voxel bone volume to total volume (VOX BV/TV) and higher trabecular number (Tb.n) with reduced trabecular separation (Tb.sp). A large magnitude effect size was observed in the levels of circulating bone formation Procollagen I N-terminal propeptide (P1NP) at day 60 of life; reabsorption cross-linked C-telopeptide of type I collagen (CTX) markers were similar between the androgenized and control rats at days 60 and 110 of life. The analysis of gene expression in bone indicated elements for an increased bone mass such as the reduction of the Dickkopf-1 factor (Dkk1) a negative regulator of osteoblast differentiation (bone formation) and the reduction of Interleukin 1-b (Il1b), an activator of osteoclast differentiation (bone reabsorption). Results from this study highlight the possible role of the developmental programming on bone microarchitecture with reference to young women with PCOS.

Download Full-text

AB1240 C4B BINDING PROTEIN AND WARFARIN IN THE ANTIPHOSPHOLIPID SYNDROME

Annals of the Rheumatic Diseases ◽

10.1136/annrheumdis-2020-eular.5606 ◽

2020 ◽

Vol 79 (Suppl 1) ◽

pp. 1911.2-1911

Author(s):

G. Grosso ◽

K. Sandholm ◽

I. Gunnarsson ◽

A. Zickert ◽

A. Vikerfors ◽

...

Keyword(s):

Antiphospholipid Syndrome ◽

Mediation Analysis ◽

Binding Protein ◽

Protein A ◽

Protein S ◽

Protein Isoforms ◽

Type I ◽

Complement Inhibitor ◽

Warfarin Treatment ◽

The Impact

Background:Complement plays a role in the Antiphospholipid Syndrome (APS). C4b Binding Protein (C4BP) is a complement inhibitor with anticoagulant function (1). It belongs to the same protein family as β2GPI, the main antigen in APS. Its main isoform is bound to protein S in the circulation. Levels of both protein S and C4BP are known to be reduced by warfarin treatment (2) as well as by aPL, directly and indirectly.Objectives:To investigate the levels of C4BP in primary (p) and secondary (s) APS, also considering warfarin treatment.Methods:The total amount of C4BP (C4BPt) was measured by using magnetic carboxylated microspheres which were coupled with a monoclonal antibody against the α-chain of human-C4BP to capture the antigen. To detect C4BPt the same antibody was used, biotinylated. The binding of biotinylated antibodies was detected by streptavidin-phycoerythrin and data were collected using a MAGPIX Multiplex Reader. Using independent t-test, we compared C4BP in 118 SLE patients with repeated positivity for Antiphospholipid antibodies (aPL) (39/118 on warfarin), 291 aPL negative SLE patients (16/291 on warfarin), 67 pAPS (33/67 on warfarin), and 322 controls (none on warfarin). We then performed an interaction and a mediation analysis (3) in the SLE group to study the impact of warfarin on C4BP levels: since warfarin is mostly prescribed to aPL+ patients, it is considered a mediator in the reducing effect of aPL on C4BP. Therefore we compared individuals exposed and non-exposed to the presence of aPL with or without the mediator warfarin and calculated the percentage of reduction in C4BP that could be attributed to aPL or warfarin.Results:Overall C4BP is 20% reduced in aPL+ patients (fig 1), independently of SLE, past thrombotic events and nephritis. Warfarin treated patients have lower levels of C4BP (fig 2). According to mediation analysis 11% of C4BP reduction is due to aPL and 9% to warfarin.Figure 1.C4BP in different subgroups (67 pAPS, 118 SLEaPL+, 291 SLEaPL-, 322 controls)Figure 2.C4BP in 67 pAPS patients, 33/67 on warfarinConclusion:Both aPL and warfarin decrease levels of C4BP, a complement and coagulation regulator. Reduction of this complement inhibitor could contribute to complement activation and thrombosis in APS. Our results raise new questions regarding the effects of warfarin treatment on complement and coagulation in APS.References:[1]Dahlbäck B. C4b-binding protein: a forgotten factor in thrombosis and hemostasis. Seminars in thrombosis and hemostasis 2011; 37(4): 355.[2]Zöller B, García de Frutos P, Dahlbäck B. Evaluation of the relationship between protein S and C4b-binding protein isoforms in hereditary protein S deficiency demonstrating type I and type III deficiencies to be phenotypic variants of the same genetic disease. Blood 1995; 85(12): 3524.[3]Vanderweele TJ, Vansteelandt S. Conceptual issues concerning mediation, interventions and composition. Statistics and Its Interface 2009; 2(4): 457-68.Disclaimer:AV is employed at the Swedish Medical Products Agency, the views expressed in this paper are the personal views of the authors and not necessarily the views of the Governement AgencyAcknowledgments:Thanks to the Biostatistics Core Facility, Karolinska UniversityDisclosure of Interests:None declared

Download Full-text

Modulatory Effect of Glycated Collagen on Oral Streptococcal Nanoadhesion

Journal of Dental Research ◽

10.1177/0022034520946320 ◽

2020 ◽

Vol 100 (1) ◽

pp. 82-89

Author(s):

C.M.A.P. Schuh ◽

B. Benso ◽

P.A. Naulin ◽

N.P. Barrera ◽

L. Bozec ◽

...

Keyword(s):

Dental Caries ◽

Biofilm Formation ◽

Type I Collagen ◽

Type I ◽

Oral Streptococci ◽

Oral Diseases ◽

Collagen Crosslinking ◽

Initial Adhesion ◽

Collagen Glycation ◽

The Impact

Biofilm-mediated oral diseases such as dental caries and periodontal disease remain highly prevalent in populations worldwide. Biofilm formation initiates with the attachment of primary colonizers onto surfaces, and in the context of caries, the adhesion of oral streptococci to dentinal collagen is crucial for biofilm progression. It is known that dentinal collagen suffers from glucose-associated crosslinking as a function of aging or disease; however, the effect of collagen crosslinking on the early adhesion and subsequent biofilm formation of relevant oral streptococci remains unknown. Therefore, the aim of this work was to determine the impact of collagen glycation on the initial adhesion of primary colonizers such as Streptococcus mutans UA159 and Streptococcus sanguinis SK 36, as well as its effect on the early stages of streptococcal biofilm formation in vitro. Type I collagen matrices were crosslinked with either glucose or methylglyoxal. Atomic force microscopy nanocharacterization revealed morphologic and mechanical changes within the collagen matrix as a function of crosslinking, such as a significantly increased elastic modulus in crosslinked fibrils. Increased nanoadhesion forces were observed for S. mutans on crosslinked collagen surfaces as compared with the control, and retraction curves obtained for both streptococcal strains demonstrated nanoscale unbinding behavior consistent with bacterial adhesin-substrate coupling. Overall, glucose-crosslinked substrates specifically promoted the initial adhesion, biofilm formation, and insoluble extracellular polysaccharide production of S. mutans, while methylglyoxal treatment reduced biofilm formation for both strains. Changes in the adhesion behavior and biofilm formation of oral streptococci as a function of collagen glycation could help explain the biofilm dysbiosis seen in older people and patients with diabetes. Further studies are necessary to determine the influence of collagen crosslinking on the balance between acidogenic and nonacidogenic streptococci to aid in the development of novel preventive and therapeutic treatment against dental caries in these patients.

Download Full-text

Proline-rich tyrosine kinase 2 mediates transforming growth factor-beta-induced hepatic stellate cell activation and liver fibrosis

Scientific Reports ◽

10.1038/s41598-020-78056-0 ◽

2020 ◽

Vol 10 (1) ◽

Author(s):

Jonghwa Kim ◽

Wonseok Kang ◽

So Hee Kang ◽

Su Hyun Park ◽

Ji Young Kim ◽

...

Keyword(s):

Liver Fibrosis ◽

Tyrosine Kinase ◽

Focal Adhesion ◽

Transforming Growth Factor ◽

Family Members ◽

Type I ◽

Tyrosine Kinase 2 ◽

The Impact ◽

Tgf Β1

AbstractHepatic fibrogenesis is characterized by activation of hepatic stellate cells (HSCs) and accumulation of extracellular matrix (ECM). The impact of ECM on TGF-β-mediated fibrogenic signaling pathway in HSCs has remained obscure. We studied the role of non-receptor tyrosine kinase focal adhesion kinase (FAK) family members in TGF-β-signaling in HSCs. We used a CCl4-induced liver fibrosis mice model to evaluate the effect of FAK family kinase inhibitors on liver fibrosis. RT-PCR and Western blot were used to measure the expression of its target genes; α-SMA, collagen, Nox4, TGF-β1, Smad7, and CTGF. Pharmacological inhibitors, siRNA-mediated knock-down, and plasmid-based overexpression were adopted to modulate the function and the expression level of proteins. Association of PYK2 activation with liver fibrosis was confirmed in liver samples from CCl4-treated mice and patients with significant fibrosis or cirrhosis. TGF-β treatment up-regulated expression of α-SMA, type I collagen, NOX4, CTGF, TGF-β1, and Smad7 in LX-2 cells. Inhibition of FAK family members suppressed TGF-β-mediated fibrogenic signaling. SiRNA experiments demonstrated that TGF-β1 and Smad7 were upregulated via Smad-dependent pathway through FAK activation. In addition, CTGF induction was Smad-independent and PYK2-dependent. Furthermore, RhoA activation was essential for TGF-β-mediated CTGF induction, evidenced by using ROCK inhibitor and dominant negative RhoA expression. We identified that TGF-β1-induced activation of PYK2-Src-RhoA triad leads to YAP/TAZ activation for CTGF induction in liver fibrosis. These findings provide new insights into the role of focal adhesion molecules in liver fibrogenesis, and targeting PYK2 may be an attractive target for developing novel therapeutic strategies for the treatment of liver fibrosis.

Download Full-text