![]() ![]() Adobe Premiere Pro is a timeline-based video editing app developed by Adobe Systems and published as part of the Adobe Creative Cloud licensing program. · Please help! How can I send my illustrator draw file from ipad to illustrator cc "pdf"? There is no possibility. There is just export through email as a jpeg!!! If you’re already familiar with Adobe’s flagship, it won’t take long to orient yourself in Affinity Photo. Lately, I have been working on some children illustrations, creating some über cute creatures. In the following easy tutorial, I’ll show you how to create a cute.Review: Affinity Photo 1. Digital Photography Review. Usually, the price of software comes at the end of the review, but with Affinity Photo 1. Mac and Windows, the price is the starting point, along with a prominent qualifier from the product’s website: 'No subscription.'Key Features. Professional editing tools for almost anyone who needs to manipulate images. Edits are mostly non- destructive. Windows and Mac support. Inexpensive, with no subscription required. Batch processing. Affinity Photo’s developer, Serif, knows its audience. When Adobe shifted Photoshop and nearly all of its other products to a subscription model in 2. Four years later, despite the move being apparently successful for Adobe, subscription pricing continues to be a point of contention for many people, turning into an opportunity for developers like Serif. If you’re already familiar with Adobe’s flagship, it won’t take long to orient yourself in Affinity Photo. However, simply offering a less expensive image editor isn’t enough. We’re beyond the point where photographers will put up with limited software to save a few bucks, and with Affinity Photo, we don’t have to. You won’t find some of the specialized features Photoshop includes, such as its 3. D tools, but most everything else is there – sometimes to Affinity Photo’s detriment. Getting Started. Software should be evaluated on its own merits, and for the most part I’m looking at Affinity Photo through that lens. How does it perform for photographers? Does it get in the way when handling familiar operations? Does it improve the editing experience? Comparisons to Photoshop inevitably come up, and I’ll refer to them when needed, but this isn’t specifically a comparative review between Affinity Photo and Photoshop. That said, if you’re already familiar with Adobe’s flagship, it won’t take long to orient yourself in Affinity Photo. If photo editing beyond the basics is new to you, it’s easy to pick up. Working modes, aka 'Personas'Affinity Photo is built around four working modes, referred to as “personas,” each of which contains its own specialized tools. These personas include: Photo, Develop, Tone Mapping and Export. The Photo persona is the main editing interface, with adjustments, layers, masks, and the like. The Liquify persona is a playground for distorting areas when retouching (creating an editable mesh of the entire image and then pushing and pulling the pixels to do things like make areas seem slimmer or to correct distortion). The Develop persona kicks in when opening a raw file for pre- processing, akin to Adobe Camera Raw. The Tone Mapping persona is exclusive for working with HDR (high dynamic range) effects, which can apply to single images as well as several merged shots. And lastly, the Export persona provides tools for creating versions of the image outside the application, from specifying file types and compression levels to preset slices. You’ll also find tools for painting and drawing, including extensive controls for creating and manipulating brushes, but for the sake of brevity, I’m looking at the application in terms of editing photos. Anti- Inflammatory Effects of Progesterone in Lipopolysaccharide- Stimulated BV- 2 Microglia. Beilei Lei,1,2. Brian Mace,3. Hana N. Dawson,3. David S. Warner,1,2,4. Daniel T. Laskowitz,1,2,3,4 and Michael L. James. 1,2,3,*Karin E. Peterson, Editor. Multidisciplinary Neuroprotection Laboratories, Duke University Medical Center, Durham, North Carolina, United States of America. Department of Anesthesiology, Duke University Medical Center, Durham, North Carolina, United States of America. Department of Neurology, Duke University Medical Center, Durham, North Carolina, United States of America. Department of Neurobiology, Duke University Medical Center, Durham, North Carolina, United States of America. National Institute of Allergy and Infectious Diseases - Rocky Mountain Laboratories, United States of America. Competing Interests: The authors have declared that no competing interests exist. Conceived and designed the experiments: BL MLJ. Performed the experiments: BL BM. Analyzed the data: BL BM MLJ. Contributed reagents/materials/analysis tools: HND DSW DTL MLJ. Contributed to the writing of the manuscript: BL HND DSW DTL MLJ. Received 2. 01. 4 Apr 1; Accepted 2. Jul 8. This article has been cited by other articles in PMC. Abstract. Female sex is associated with improved outcome in experimental brain injury models, such as traumatic brain injury, ischemic stroke, and intracerebral hemorrhage. This implies female gonadal steroids may be neuroprotective. A mechanism for this may involve modulation of post- injury neuroinflammation. As the resident immunomodulatory cells in central nervous system, microglia are activated during acute brain injury and produce inflammatory mediators which contribute to secondary injury including proinflammatory cytokines, and nitric oxide (NO) and prostaglandin E2 (PGE2), mediated by inducible NO synthase (i. NOS) and cyclooxygenase- 2 (COX- 2), respectively. We hypothesized that female gonadal steroids reduce microglia mediated neuroinflammation. In this study, the progesterone’s effects on tumor necrosis factor alpha (TNF- α), i. NOS, and COX- 2 expression were investigated in lipopolysaccharide (LPS)- stimulated BV- 2 microglia. Further, investigation included nuclear factor kappa B (NF- κB) and mitogen activated protein kinase (MAPK) pathways. LPS (3. 0 ng/ml) upregulated TNF- α, i. NOS, and COX- 2 protein expression in BV- 2 cells. Progesterone pretreatment attenuated LPS- stimulated TNF- α, i. NOS, and COX- 2 expression in a dose- dependent fashion. Progesterone suppressed LPS- induced NF- κB activation by decreasing inhibitory κBα and NF- κB p. Progesterone decreased LPS- mediated phosphorylation of p. Jun N- terminal kinase and extracellular regulated kinase MAPKs. These progesterone effects were inhibited by its antagonist mifepristone. In conclusion, progesterone exhibits pleiotropic anti- inflammatory effects in LPS- stimulated BV- 2 microglia by down- regulating proinflammatory mediators corresponding to suppression of NF- κB and MAPK activation. This suggests progesterone may be used as a potential neurotherapeutic to treat inflammatory components of acute brain injury. Introduction. Numerous studies indicate that progesterone regulates multiple non- reproductive functions in the brain including cognition, memory, and neurogenesis [1], [2], [3], [4]. Progesterone elicits its effects via progesterone receptors (PRs), which include classical nuclear PRs (two major isoforms PR- A and PR- B) and recently recognized membrane PRs [3], [5], [6], [7]. The classical mechanism of progesterone action is mediated by nuclear PRs, which function as transcription factors by binding to specific progesterone response elements within the promoter region of target genes to modulate transcription and genomic networks [3], [4], [8]. Non- classical mechanisms have been recently suggested to involve membrane PRs and cytoplasmic kinase activation and signal cascades [3], [4], [8]. Progesterone exerts neuroprotective effects in several experimental acute brain injury models, including traumatic brain injury [9], [1. Progesterone has also demonstrated potential for clinical translation, having shown promise for treatment of traumatic brain injury in two independent phase II clinical trials [2. III clinical trials (http: //clinicaltrials. NCT0. 08. 22. 90. NCT0. 08. 22. 90. NCT0. 08. 22. 90. Preclinical studies suggest that progesterone may improve neurobehavioral outcomes by inhibition of neuroinflammation, oxidative stress, and neuronal death [1. However, specific underlying mechanisms remain unclear. Microglia, the resident immune cells in the central nervous system, play important roles in the brain’s innate immunity and response to injury. Increasing evidence indicates microglial over- activation after acute brain injury results in excess production of proinflammatory mediators including tumor necrosis factor α (TNFα), prostaglandin E2 (PGE2), and nitric oxide (NO), which then contribute to secondary brain injury and exacerbate neuronal injury [2. NO and PGE2 are the products of inducible nitric oxide synthase (i. NOS) and cyclooxygenase- 2 (COX- 2), respectively. Regulation of i. NOS, COX- 2 and TNFα expression involves transcriptional factor nuclear factor kappa B (NF- κB) [2. MAPKs) [3. 2], [3. Lipopolysaccharide (LPS), a toll- like receptor ligand, induces microglia activation and neuroinflammation. The immortalized murine BV- 2 microglia cell line is commonly used as a substitute for primary microglia in experimental studies [3. To investigate progesterone’s molecular effects on neuroinflammation, BV- 2 microglia cells were employed to test the effects of progesterone on the LPS- induced TNF- α, i. NOS, and COX- 2 expression. Since both NF- κB and MAPK pathways participate in the regulation of neuroinflammation [2. Materials and Methods. Materials. Reagents and suppliers were: LPS (L6. P8. 78. 3), mifepristone (M8. Sigma, St. Louis, MO); High Glucose Dulbecco’s Modified Eagle Medium (DMEM) (1. DMEM (3. 10. 53), L- glutamine, sodium pyruvate, Pen/Strep and fetal bovine serum (Gibco, Grand Island, NY); NE- PER nuclear and cytoplasmic extraction reagents (7. BCA protein assay kit (2. Thermo Scientific, Rockford, IL); mouse TNF- α Duo. Set enzyme- linked immunosorbent assay (ELISA) kit (DY4. R& D Systems, Minneapolis, MN); Antibodies against NF- κB p. NF- κB (3. 03. 3), IκB- α (9. IκBα (9. 24. 6), p. MAPK, p. 44/4. 2 (9. MAPK, JNK (9. 25. JNK (9. 25. 1), GAPDH (2. Cell signaling, Beverly, MA); COX- 2 antibody (1. Cayman chemical, Ann Arbor, MI); antibodies against progesterone receptor (sc- 7. NOS2 (sc- 6. 50) and secondary HRP antibodies (Santa Cruz Biotechnology, Santa Cruz, CA). Cell culture. BV- 2, an immortalized mouse microglia cell line [3. DMEM supplemented with 1. FBS and 1x penicillin/streptomycin in a humidified atmosphere containing 5% CO2 at 3. C. Immunofluorescence staining. Cells were grown on glass coverslips in complete medium for one day. After aspiration of medium, cells were fixed at room temperature for 1. PBS, permeablized in the same solution with 0. Triton X- 1. 00 for 1. PBS before 3. 0 min of blocking in 1. FBS/PBS with 0. 0. Triton X- 1. 00, and then incubated with primary antibodies to progesterone receptor (1∶1. C in blocking buffer. After washing with PBS 3 times, cells were incubated at 2. C for 3. 0 min with secondary goat anti- rabbit Ig. G Rhodamine Red X (Invitrogen) at 1∶1. PBS, mounting with anti- fading buffer with DAPI and fluorescent microscopy analysis. Images were processed with Adobe Photoshop software (Adobe Systems Inc., San Jose, CA). Treatments. Prior to all experiments, BV- 2 cells near confluence were trypsinized and plated in 1. DMEM for 1 day, and then washed and transferred to serum free and no phenol red DMEM with 1x L- glutamine and 1x sodium pyruvate for treatment. For time course experiments, cells were incubated with 3. LPS for different time periods from 0 to 2. Pretreatment of escalated concentrations of progesterone (1. M) was given 1 h before addition of 3. LPS. Post- treatment with progesterone was given 5, 3. LPS. In additional experiments, the progesterone receptor antagonist mifepristone (1. M) was given 3. 0 min before progesterone. At pre- specified time points, cell supernatants were collected for TNF- α ELISA, and cells were lysed for western blot analyses. Quantification of TNF- αCell supernatants were collected and spun at 1.
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