References30.99 · Dr kulvinder kaur centre for human reproduction,Jalandhar,Punjab,India.34.72 · Rotunda Center For Human ReproductionAbstractHeparin is normally physiologically produced by mast cells in the body.Recently low molecular weight heparins have been shown to be useful in prevention of recurrent miscarriages ,intrauterine growth retardation,preeclampsia,abruption placentae and low birth weight.This minireview summarizes the recent advances of roles of endocannabinoid ,prokineticin signaling,role of mast cells in reproduction and implantation and how various in vitro studies suggest that low molecular weight heparins(LMWH) have an effect in improving implantation in nonthrombophilia patients besides improving in thrombophiliacs thereby suggesting it may be time to check a role for routine use of LMWH by multicenter trials in improving success rates of IVF worldwide.Discover the world's research11+ million members100+ million publications100k+ research projects
ABSTRACT: Prokineticin 1 (PROK1) signalling via prokineticin receptor 1 (PROKR1) regulates the expression of several genes with important roles in endometrial receptivity and implantation. This study investigated PROK1 regulation of Dickkopf 1 (DKK1) expression, a negative regulator of canonical Wnt signalling, and its function in the non-pregnant endometrium and first trimester decidua. DKK1 mRNA expression is elevated during the mid-secretory phase of the menstrual cycle and expression increases further in first trimester decidua. DKK1 protein expression is localized to glandular epithelial and stromal cells during the proliferative, early- and mid-secretory phases, whereas expression is confined to the stroma in the late-secretory phase and first trimester decidua. PROK1 induces the expression of DKK1 in endometrial epithelial cells stably expressing PROKR1 and in first trimester decidua explants, via a Gq-calcium-calcineurin-nuclear factor of activated T-cells-mediated pathway. Endometrial epithelial cell proliferation is negatively regulated by PROK1-PROKR1 signalling. We demonstrate that this effect on cell proliferation occurs via DKK1 expression, as siRNA targeted against DKK1 reduces the PROK1-induced decrease in proliferation. Furthermore, decidualization of primary human endometrial stromal cells with progesterone and cyclic adenosine monophosphate is inhibited by miRNA knock down of PROK1 or DKK1. These data demonstrate important roles for PROK1 and DKK1 during endometrial receptivity and early pregnancy, which include regulation of endometrial cell proliferation and decidualization. Full-text · Article · May 2011 +2 more authors ...ABSTRACT: It is unclear how IGFs become separated from their IGF-binding proteins (IGFBPs) in vivo. However, the IGFBPs possess binding sites for glycosaminoglycans (GAGs) and interaction with GAGs alters IGFBP ligand affinity. Accordingly, GAGs may control IGF bioavailability. To test this hypothesis, we investigated the effect of GAGs on serum levels of free and bioactive IGF-I, total IGF-I, and IGFBPs in vitro.
Serum was incubated with increasing concentrations of six different GAGs (heparin, tinzaparin (Innohep), dermatan sulfate, heparan sulfate, non-anticoagulant (nac) heparin, and nac low-molecular weight heparin). To investigate for reversibility, heparin was co-incubated with protamine sulfate (PS). Finally, the effect of heparin was studied in serum from pregnant and post partum women, normal subjects and patients with type 1 diabetes.
All GAGs increased free IGF-I in a dose-dependent manner (P&0.0001), whereas total IGF-I and IGFBP levels remained unchanged. However, the potency of the GAGs differed significantly (P&0.0001) and did not relate to their anti-coagulating activity. The effect of heparin on free IGF-I was fully reversed by PS. Heparin increased free and bioactive IGF-I in all tested sera (P&0.0001), but the increase was most pronounced in samples from pregnant women (P&0.0001).
All tested GAGs stimulated the release of free and bioactive IGF-I in several types of serum, most likely by reversible interaction with the IGFBPs. The effect was most pronounced in pregnancy sera, which are characterized by extensive IGFBP-3 proteolysis. Our findings support the view that GAGs localized in the vessel wall and attached to the extracellular matrix control IGF-I tissue accessibility and bioactivity. Full-text · Article · Aug 2006 +3 more authors ...ABSTRACT: Endocannabinoids are an emerging class of lipid mediators, which mimic several effects of cannabinoids. Anandamide (arachidonoylethanolamide) is a major endocannabinoid, which has been shown to impair pregnancy and embryo development. The activity of anandamide is controlled by cellular uptake through a specific transporter and intracellular degradation by the enzyme anandamide hydrolase (fatty acid amide hydrolase, FAAH). We characterized FAAH in mouse uterus by radiochromatographic and immunochemical techniques, showing that the enzyme is confined to the epithelium and its activity decreases appreciably during pregnancy or pseudopregnancy because of lower gene expression at the translational level. Ovariectomy prevented the decrease in FAAH, and both progesterone and estrogen further reduced its basal levels, suggesting hormonal control of the enzyme. Anandamide was shown to induce programmed cell death in mouse blastocysts, through a pathway independent of type-1 cannabinoid receptor. Blastocysts, however, have a specific anandamide transporter and FAAH, which scavenge this lipid. Taken together, these results provide evidence of an interplay between endocannabinoids and sex hormones in pregnancy. These findings may also be relevant for human fertility, as epithelial cells from healthy human uterus showed FAAH activity and expression, which in adenocarcinoma cells was increased fivefold. Full-text · Article · Jun 2000 +2 more authors ...ArticleFebruary 2017 · Health reports / Statistics Canada, Canadian Centre for Health Information = Rapports sur la santé / Statistique Canada, Centre canadien d'information sur la santé · Impact Factor: 2.67ArticleFebruary 2017 · Rheumatology (Oxford, England) · Impact Factor: 4.47+7 more authors…ArticleFebruary 2017 · Clinical and experimental obstetrics & gynecology · Impact Factor: 0.42ArticleFebruary 2017+3 more authors…Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.This publication is from a journal that may support self archiving.
oror log in withWorkaround for a Pantone Plus selection glitch in CS6 - InDesignSecrets : InDesignSecrets
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July 5, 2012
A newly-minted InDesign CS6 user e-mailed us this query:
I wanted to see if there is a way to change the display of the Pantone Plus book colours instead of by colour/grouping, listing them numerically. If you try to type certain numbers in it, you can’t find them (ie: 543 always defaults to 5435 and you aren’t allowed to change it/delete the additional ). Any assistance would be greatly appreciated.
Unfortunately, I can’t see any way to change the order of the swatches in any of the color libraries in the New Swatch dialog box. My guess is that since they’re embedded in a dialog box (as opposed to a panel, as in Illustrator, where you can sort a library’s swatches by name), InDesign can’t really provide that flexibility.
It is frustrating that in earlier versions, though, you could enter  in the Pantone spot color Find field to get Pantone 543, and &#” to get 5435; but you can’t in CS6-as you said, it always jumps to 5435. The only way I was able to find Pantone 543 in the screen shot below was by typing  and then using my up and down arrow keys for a few minutes until I found the sucker.
I believe this is a bug with the new Pantone+ libraries in InDesign CS6, and hope that it’s something easily fixed in an upcoming patch.
In the meantime, I have a somewhat drastic, but I believe safe, workaround: Add an older version Pantone swatch library back into the program, and use that to select your spot color.
Adding back an older Pantone swatch library
Before I get to the how-to on adding a swatch library to InDesign CS6 (and it’s quite simple), let me explain. The main difference between the older Pantone libraries and the new Pantone+ ones in InDesign CS6 is how the spot colors are defined internally for on-screen display: as CMYK (old version) or Lab (new Plus version). The Lab values, having a wider gamut, give a more accurate preview on screen. Illustrator has been using Lab values for its Pantone spot colors since CS2.
For the past few versions of InDesign, you could (and still can) make the older Pantone swatches use Lab definitions by choosing “Use standard Lab values for Spots” in the Ink Manager (available in the Swatches panel menu). When InDesign is using the Lab values, a little icon indicating a Lab color next to the spot color icon appears – here it is in close-up:
The Lab color definition is also used if you convert your spot colors to process, or if objects filled with a spot color are part of certain transparency effects. If you’re working in a tightly managed color workflow, you’ll need to pay attention to these kinds of things. But if all you’re doing is using a spot for a spot, when you print out CMYK + spot separations, it makes no difference how things looked on screen. Whether Pantone 5435 is defined to display onscreen as Lab or as CMYK, either will end up on the same separation plate and be the same exact ink on paper.
Okay, now let’s move on to the how-to: I found a wonderful Adobe help document all about Pantone Plus, aimed at Illustrator users, that also has instructions for InDesign users. It’s called , and instructs Illustrator (and InDesign) users how to replace the newer Lab-based Pantone libraries with the older CMYK-based ones. (I would never recommend that personally, but I suppose if for some reason that’s the only solution for your workflow, it’d be a relief to know how to to switch back.)
What’s great is that for our purposes, this Help file has a ZIP file of the Pantone libraries, so we don’t have to use the Pantone Color Manager application (a bit problematic) to fiddle with our swatch libraries, we can just drag and drop them manually. Look at that
online document, about 2/3 of the way down (at the end of its “Workaround 1” instructions), and you’ll find a link to the older Pantone swatch libraries, . Download that zip file, extract the contents, and copy over just the libraries you need to your InDesign application folder.
The “Workaround 1: Adobe InDesign CS6” steps in the Help file show you exactly where the files should go, so follow their instructions. Remember though that the instructions are all about replacing files, but we’re not doing that .. .just adding them. The filenames are different so there’s no worries. The new ones you add appear at the bottom of the list. Here I added PANTONE solid coated and PANTONE solid matte, the spot libraries I use 99% of the time:
Now if I find I’m fighting with an overly zealous autocomplete in CS6’s Pantone swatch picker, I can just quickly switch to the older Pantone library at the bottom of the dropdown menu. In that library, I can enter  in the spot color Find field and get Pantone 543, simple as that. (Remember, it’s the same color as the Pantone+ library!) If I want Pantone 5435, I can use either the Pantone+ or the older Pantone library.
To keep things consistent, make sure InDesign always uses Lab values for spots by enabling that checkbox in the Ink Manager. Do this with no documents open so it becomes an application default.
Anne-Marie “Her Geekness” Concepción is the co-founder (with David Blatner) and CEO of , which produces InDesignSecrets, InDesign Magazine, and other resources for creative professionals. Through her cross-media design studio, , Anne-Marie develops ebooks and trains and consults with companies who want to master the tools and workflows of digital publishing. She has authored over 20 courses
on these topics and others. Keep up with Anne-Marie by subscribing to her ezine, , and contact her by email at
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