Podcasts about 125i

#125I used to have a lot of social anxiety and was afraid of how people perceived me. I didn't think I was cool or interesting, and I didn't think people would like me. Before going out, I would always have so much anxiety because I didn't know how to talk to people or what to talk about. In today's episode, I share tips on how to be more confident and become the most interesting woman in the room. DO THE INNER WORKDRESS FOR YOUBE CONFIDENT IN WHO YOU AREDON'T BE AFRAID TO BE SEENBE BOLD AND UNAPOLOGETICALLY YOUSKIP THE SMALL TALK AND BE OPEN AND REALASK PEOPLE ABOUT THEMBE KIND NOT JUST FRIENDLYBE SELECTIVE ABOUT WHO HAS ACCESS TO YOUTrying Not to Care is sponsored by Zocdoc - Go to zocdoc.com/TNTC to find and instantly book a top-rated doctor today Trying Not to Care is sponsored by Hero Bread - Get 10% off your order at hero.co and use code TNTC at checkout Trying Not to Care is sponsored by ZitSticka - Get 30% off on Amazon with code PATCHES30Trying Not to Care is sponsored by DIME Beauty - Go to DIMEBeautyco.com and get 25% off site wide during their Anniversary Sale!SOCIALS AND LINKSInstagram: Ashley's Instagram | Trying Not to Care InstagramTikTok: Ashley's TikTok | Trying Not to Care TikTokYoutube: Subscribe hereRevolve, Amazon Storefront and more: LTXIf you want to ask me questions, need advice or have any episode ideas, submit here: TNTC Community Google FormTNTC COMMUNITY GROUPCHAT: https://app.geneva.com/invite/4939298b-477b-4d4b-a32a-0b82431273bfBusiness Inquiries - ashleycorbo@dulcedo.com / ashleychristinecorbo@gmail.comProduced by Dear MediaSee Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.

Du erreichst deine Ziele nicht, auch wenn du dich noch so sehr bemühst? Dann liegt das höchstwahrscheinlich an deiner schlechten Organisation. Wie du von chaotisch und unproduktiv zu einer top organisierten Frau wirst - DAS erfährst du in diesem Video. Viel Spaß! Love you, Sophia xoxo _______________________ ___

Ask God For Discernment And Clarity Will Follow, But Remember It Will Always Be At His Pace Psalm 119:124-125 124Deal with your servant according to your love and teach me your decrees. 125I am your servant; give me discernment that I may understand your statutes.

Where Do You Get Your Discernment? Psalm 119:124 - 125 124Deal with your servant according to your love and teach me your decrees. 125I am your servant; give me discernment that I may understand your statutes.

Episode 347 is an updated guide to somatropic hormone and GOD did I go crazy on this one! I honestly want to know more about growth hormone than anyone alive and thus, begins this string of GH based guides! I DID finally discuss the MoA for how GH causes localized fat loss which really had me excited since no one in our industry has EVER talked about this so that definitely was an interesting avenue to go down! Below I am going to reference a lot of the literature for this hormone that I was read through over the past few years on this topic so please DO NOT TAKE MY WORD FOR THIS - READ THESE YOURSELF! Keep in mind this is a brief snippet of every bit of literature on the topic however. REFERENCES   Daughaday WH, Rotwein P. Insulin-like growth factors I and II. Peptide, messenger ribonucleic acid and gene structures, serum, and tissue concentrations. Endocr Rev. 1989;10:68–91. [PubMed] [Google Scholar] Jones JI, Clemmons DR. 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Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.06.11.145466v1?rss=1 Authors: Epstein, M., Maxwell, S., Piggot, T. J., Beeson, D., Bermudez, I., Biggin, P. C. Abstract: Muscle nicotinic acetylcholine receptors are a class of heteropentameric ligand-gated cation channels with constituent subunits adopting a fixed stoichiometric arrangement. The specific amino acid residues that govern subunit ordering are however, only partially understood. By integrating all-atom molecular dynamics simulations, bioinformatics, two-electrode voltage clamp electrophysiology and 125I--bungarotoxin assays of chimeric nAChR subunits, we identify residues across the extracellular, transmembrane and extended M4 helix of the {delta} subunit that make structural signatures that contribute to intransigent assembly rules. Furthermore, functional differences observed in 2{delta}2{beta} receptors can be rationalized by changes in dynamical behavior that manifest themselves at the agonist binding site. Copy rights belong to original authors. Visit the link for more info

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Having God’s wisdom and knowledge isn’t as hard to gain as what we think it is. We will never be as wise or have a full understanding as God, but that doesn’t mean we can’t learn from Him or that He won’t help us navigate life and business.I want to start with 1 John 2:18-2718 Dear children, this is the last hour; and as you have heard that the antichrist is coming, even now many antichrists have come. This is how we know it is the last hour. 19 They went out from us, but they did not really belong to us. For if they had belonged to us, they would have remained with us; but their going showed that none of them belonged to us.20 But you have an anointing from the Holy One, and all of you know the truth.[e] 21 I do not write to you because you do not know the truth, but because you do know it and because no lie comes from the truth. 22 Who is the liar? It is whoever denies that Jesus is the Christ. Such a person is the antichrist—denying the Father and the Son. 23 No one who denies the Son has the Father; whoever acknowledges the Son has the Father also.24 As for you, see that what you have heard from the beginning remains in you. If it does, you also will remain in the Son and in the Father. 25 And this is what he promised us—eternal life.26 I am writing these things to you about those who are trying to lead you astray. 27 As for you, the anointing you received from him remains in you, and you do not need anyone to teach you. But as his anointing teaches you about all things and as that anointing is real, not counterfeit—just as it has taught you, remain in him.In verse 27 it shows us that because we have the anointing because we have the Holy Spirit, He is the one that teaches us. So, if you have accepted Jesus Christ as your saviour you’ve already done the hardest yet easiest part of gaining wisdom and discernment because you have the Holy Spirit living inside of you who can teach you and give you an understanding of what God’s peace is.So next let’s look at what the wisest King in the Old TEstiment of the bible asked and see what we can learn from him…1 Kings 3:7-147 “Now, Lord my God, you have made your servant king in place of my father David. But I am only a little child and do not know how to carry out my duties. 8 Your servant is here among the people you have chosen, a great people, too numerous to count or number. 9 So give your servant a discerning heart to govern your people and to distinguish between right and wrong. For who is able to govern this great people of yours?”10 The Lord was pleased that Solomon had asked for this. 11 So God said to him, “Since you have asked for this and not for long life or wealth for yourself, nor have asked for the death of your enemies but for discernment in administering justice, 12 I will do what you have asked. I will give you a wise and discerning heart, so that there will never have been anyone like you, nor will there ever be. 13 Moreover, I will give you what you have not asked for—both wealth and honor—so that in your lifetime you will have no equal among kings. 14 And if you walk in obedience to me and keep my decrees and commands as David your father did, I will give you a long life.”God was happy that Solomon asked for God’s wisdom and because of that, He gave Him God’s wisdom plus more… It’s ok for you to ask for God’s wisdom. In your prayer time ask for this wisdom.Then if we look at James 1:2-82 Consider it pure joy, my brothers and sisters,[a] whenever you face trials of many kinds, 3 because you know that the testing of your faith produces perseverance. 4 Let perseverance finish its work so that you may be mature and complete, not lacking anything. 5 If any of you lacks wisdom, you should ask God, who gives generously to all without finding fault, and it will be given to you. 6 But when you ask, you must believe and not doubt, because the one who doubts is like a wave of the sea, blown and tossed by the wind. 7 That person should not expect to receive anything from the Lord. 8 Such a person is double-minded and unstable in all they do.Again we are told that if we lack wisdom then to ask for it.King David also asks in Psalm 119:125I am your servant; give me discernmentthat I may understand your statutes.And that leads me on to our last verse and that’s Romans 12:1-2Therefore, I urge you, brothers and sisters, in view of God’s mercy, to offer your bodies as a living sacrifice, holy and pleasing to God—this is your true and proper worship. 2 Do not conform to the pattern of this world, but be transformed by the renewing of your mind. Then you will be able to test and approve what God’s will is—his good, pleasing and perfect will.Today let’s pray and ask the Holy Spirit for God’s wisdom & discernment.Other bible verse you might find useful…1 Corinthians 14:331 John 2:271 Kings 3:91 Samuel 16:7Hebrews 5:14James 1:5Matt 10:16Proverbs 15:14 & 18:15Psalm 119:125Romans 12:2Are you ready to join a community like no other?We’ve created a sisterhood of Christian women in business who are completely in love with God and encourage each other on a daily basis with their businesses. If you’re after some Godly support as you grow your business…We invite you to become a part of this amazing, heart felt community by clicking the button below

The role of hCG as a stimulator of the human thyroid has been a subject of controversy, because discrepant results have been obtained in different in vitro assays. In an attempt to explain the variation observed in the thyroid response to hCG, we investigated the ability of hCG and that of its isoforms and glycosylation variants to inhibit [125I]bovine (b) TSH binding and stimulate adenylate cyclase in two clones, JP09 and JP26, of Chinese hamster ovary cells stably transfected with the human TSH receptor (hTSHr). The two clones differed with respect to the number of hTSHr expressed per cell (34,000 in JP09 and 2,000 in JP26 cells). Both responded extremely well to bTSH; the cAMP response to 0.001 IU/L bTSH was distinguishable from basal values. Interestingly, JP09 cells were readily stimulated by hCG (20-100 mg/L; 0.52-2.6 x 10(-6) mol/L) to release cAMP, whereas JP26 cells showed little if any response. Also, cAMP stimulation produced by asialo-hCG was 12-fold in JP09 cells and only 4-fold in JP26 cells compared to 45- and 67-fold stimulations by bTSH, respectively. Stimulation by asialo-hCG was approximately 30% that of bTSH in JP09 cells, but less than 6% in JP26 cells. When assessing the thyrotropic activity of the microheterogeneous isoforms of hCG, more alkaline pI forms were found to be more active than those of a more acidic pI regardless of whether they were derived from normal or molar pregnancy urine. Further studies with hCG, asialo-hCG, asialoagalacto-hCG, and deglycosylated hCG revealed that removal of sialic acid caused a marked increase in both its affinity for hTSHr and its cAMP-releasing potency, whereas removal of further carbohydrate, although it slightly enhanced receptor binding, was detrimental to adenylate cyclase activation. In conclusion, differences in hTSHr expression may cause a variation in the cAMP response to hCG or its glycosylation variants, as does the microheterogeneity of the hormone itself. These mechanisms may be responsible at least in part for the divergent responses of different cell types to hCG and render interpretation of the physiological meaning of the data obtained in recombinant receptor systems difficult.

Glimepiride is a novel sulfonylurea for the treatment of type II-diabetic patients exhibiting different receptor binding kinetics to β-cell membranes with 8–9-fold higher koff rate and 2.5–3-fold higher kon rate compared to glibenclamide (see accompanying paper (Müller, G. et al. (1994) Biochim. Biophys. Acta 1191, 267–277)). To elucidate the molecular basis for this differential behaviour of glimepiride and glibenclamide, direct photoaffinity labeling studies using β-cell tumor membranes were performed. [3H]Glimepiride was specifically incorporated into a membrane polypeptide of Mr = 65000 under conditions, which led to predominant labeling of a 140 kDa protein by [3H]glibenclamide (Kramer, W. et al. (1988) FEBS Lett. 229, 355–359). Labeling of the 140 kDa protein by [3H]glibenclamide was inhibited by unlabeled glimepiride and, vice versa, glibenclamide inhibited labeling of the 65 kDa protein by [3H]glimepiride. The 65 kDa protein was also specifically photolabeled by the sulfonylurea [125I]35623, whereas an 4-azidobenzoyl derivative of glibenclamide, N3-[3H]33055, exclusively labeled a 33 kDa protein. Competitive Scatchard analysis of [3H]glimepiride-binding and [3H]glibenclamide-binding to RINm5F cell membranes using glibenclamide and glimepiride, respectively, as heterologous displacing compounds yielded non-linear plots. These findings may be explained by cooperative interactions between the 140 and 65 kDa sulfonylurea-binding proteins. The possibility that sulfonylureas of different structure have different access to the 140 and 65 kDa receptor proteins due to the β-cell membrane barrier was investigated by photoaffinity labeling of solubilized β-cell membrane proteins. Interestingly, solubilization of β-cell tumor membranes led to a shift of specific [3H]glibenclamide binding from the 140 kDa to the 65 kDa binding protein, exclusively, and to an increased labeling of the 65 kDa protein by [3H]glimepiride. The labeling of a unique protein is in agreement with similar Kd values measured for both sulfonylurcas upon solubilization of β-cell tumor and RINm5F cell membranes (see accompanying paper). Furthermore, competitive Scatchard plots of [3H]glimepiride binding to solubilized RINm5F cell membrane proteins in the presence of glibenclamide and vice versa approximate linearity suggesting loss of cooperativity between the 140 kDa glibenclamide-binding and 65 kDa glimepiride-binding proteins upon solubilization. The physiological significance of the differential interaction of glimepiride and glibenclamide with different binding proteins was also substantiated by photoaffinity labeling of RINm5F cells leading to labeling of a 140 kDa protein by [3H]glibenclamide and of a 65 kDa protein by [3H]glimepiride. In conclusion, this report presents the first evidence that different sulfonylurea drugs bind to different components of the sulfonylurea receptor complex which are characterized by different accessibility for the drugs.

There is increasing evidence for rapid steroid action on electrolyte transport in human mononuclear leukocytes (HML). In HML, aldosterone stimulates the Na+/H+ antiporter within a few minutes. Because a variety of hormones and growth factors activate the Na+/H+ antiporter via protein kinase C and inositol phospholipids, a possible involvement of inositol-1,4,5-trisphosphate (IP3) in the rapid effects of aldosterone in HML was investigated. The stimulation of IP3 generation was started by the addition of aldosterone, concanavalin A, or other steroids. A significant increase in IP3 levels by aldosterone (1 nmol/L, P < 0.05) was found after 1 min, similar to that found after concanavalin A (25 micrograms/mL). Aldosterone caused a concentration-dependent elevation of IP3 levels, with an apparent EC50 of approximately 0.1 nmol/L. Fludrocortisone stimulated IP3 generation at similar concentrations, whereas a weaker IP3 stimulation by glucocorticoids (hydrocortisone, dexamethasone) occurred at micromolar concentrations only. Canrenone, a potent inhibitor of classical aldosterone action, was not effective up to a concentration of 100 nmol/L. These findings show kinetic and pharmacological similarities with both the functional data on Na+/H+ antiport stimulation by aldosterone and the studies of 125I-aldosterone binding to plasma membranes of HML. Thus, these data are the first to indicate an involvement of the phosphoinositide pathway in the rapid membrane effects of aldosterone.

The plasmid-encoded outer membrane protein YadA of enteropathogenic yersiniae is associated with pathogenicity. Recently, collagen binding of YadA-positive yersiniae was reported without detailed characterization (L. Emödy, J. Heesemann, H. Wolf-Watz, M. Skurnik, G. Kapperud, P. O'Toole, and T. Wadström, J. Bacteriol. 171:6674-6679, 1989). To elucidate the nature of collagen binding to YadA, we used a recombinant Yersinia strain expressing the cloned YadA gene. Direct binding of YadA-positive yersiniae to collagens was demonstrated in affinity blot experiments on nitrocellulose filters. A spectrum of collagen types in a wide concentration range were tested for their ability to block binding of 125I-labeled collagen type II to YadA-positive yersiniae. The results indicate a specific binding site(s) for YadA in collagen types I, II, III, IV, V, and XI. In contrast, collagen type VI did not bind to YadA. To characterize the binding site(s) more precisely, isolated collagen chains and cyanogen bromide fragments were investigated. These studies revealed that binding of YadA to collagen type I is confined to the alpha 1(I) chain, whereas the binding site within collagen type XI is localized in the alpha 3(XI) chain. alpha 2(I), alpha 1(XI), and alpha 2(XI) did not bind to YadA. Most interestingly, in the alpha 1(II) chain the specific binding site for YadA resides in the cyanogen bromide fragment CB10. The latter might indicate a binding site that does not depend on conformation. Based on these findings, further fragmentation and the synthesis of peptides may allow definition of the peptide sequence(s) relevant for YadA binding.

A highly sensitive radioimmunossay for arginine8-vasopressin (argipressin; INN) measurement was developed using Amberlite XAD 2 resin columns to extract arginine8-vasopressin from acidified human plasma. Arginine8-vasopressin was determined by a rapid radioimmunoassay method (2 x 20 h) using a specific antibody and 125I-labelled antigen. The bound fraction was separated by adsorption of the free fraction onto bovine serum albumin-coated charcoal; this resulted in low unspecific binding of less than 2%. Recovery experiments in the physiological range resulted in a mean (+/- SEM) recovery of 88 +/- 3%. The radioimmunoassay consistently yielded a detection limit of 0.3 ng/l (ED90) and a mean 50% binding intercept (ED50) of 3.5 ng/l. Arginine8-vasopressin immunoreactivity was characterized by reverse-phase high performance liquid chromatography, which confirmed the specificity of the assay. Serial plasma dilution curves paralleled the standard curve. The intra- and inter-assay variations were 9.4% and 15%, respectively. Arginine8-vasopressin concentrations in healthy subjects were determined in normal hydration status (2.2 +/- 0.3 ng/l; n = 11), as well as during suppression by water immersion (1.5 +/- 0.2 ng/l; n = 11) or by water loading (1.6 +/- 0.2 ng/l; n = 8). Thus, this assay allows for a sensitive, accurate and rapid quantification of plasma arginine8-vasopressin concentrations.

The insulin like growth factor-II/mannose-6-phosphate (IGF-II/M6P) receptor has been detected in many cells and tissues. In the rat, there is a dramatic developmental regulation of IGF-II/M6P receptor expression, the receptor being high in fetal and neonatal tissues and declining thereafter. We have systematically studied the expression of the human IGF-II/M6P receptor protein in tissues from 10 human fetuses and infants (age 23 weeks gestation to 24 months postnatal). We have asked 1) whether there is differential expression among different organs, and 2) whether or not the human IGF-II/M6P receptor is developmentally regulated from 23 weeks gestation to 24 months postnatal. Protein was extracted from human tissues using a buffer containing 2% sodium dodecyl sulfate and 2% Triton X-100. Aliquots of the protein extracts were analyzed by sodium dodecyl sulfate- polyacrylamide gel electrophoresis and immunoblotting using an anti-IGF- II/M6P receptor antiserum (no. 66416) and 125I-protein A or an immunoperoxidase stain. IGF-II/M6P receptor immunoreactivity was detected in all tissues studied with the highest amount of receptor being expressed in heart, thymus, and kidney and the lowest receptor content being measured in brain and muscle. The receptor content in ovary, testis, lung, and spleen was intermediate. The apparent molecular weight of the IGF-II/M6P receptor (220,000 kilos without reduction of disulfide bonds) varied among the different tissues: in brain the receptor was of lower molecular weight than in other organs. Immunoquantitation experiments employing 125I-protein A and protein extracts from human kidney at different ages revealed a small, albeit not significant, difference of the receptor content between fetal and postnatal tissues: as in other species, larger amounts of receptor seemed to be present in fetal than in postnatal organs. In addition, no significant difference of the receptor content between human fetal liver and early postnatal liver was measured employing 125I-protein A- immunoquantitation in three fetal and five postnatal liver tissue samples. The distribution of IGF-binding protein (IGEBP) species, another abundant and major class of IGF binding principles, was also measured in human fetal and early postnatal lung, liver, kidney, muscle, and brain using Western ligand blotting with 125I-IGF-II: as with IGF-II/M6P receptor immunoreactivity there was differential expression of the different classes of IGFBPs in the various organs.