Podcasts about conclusion thus

Part III of "Christianity or the Church?" Read the text here: http://orthodoxinfo.com/inquirers/sthilarion_church.aspx 0:00 St. Irenaeus on how Christ's incarnation is not about teaching but about man becoming a new creation in Christ 1:26 If Christ is only a teacher he is not very original 2:18 “The essence of Christ's activities, as we have seen, is not at all in teaching, but in salvation.” 4:13 People seeking life from the Bible and not the Church are like Adam and Eve seeking life from the apple and not from the God-Man 5:25 Leo Tolstoy, the infamous preacher of churchless Christianity in Russia 7:10 Tolstoy also denied the Holy Spirit, calling the Church “the Holy Spirit's” and not Christ's 8:35 At least Tolstoy showed us the logical conclusion of separating Christ's salvific acts from his teaching 10:00 The example of Tolstoyism shows that churchless Christinaity even destroys Christiniaty itself, but not the Church, refuted by its own lifelessness 10:40 What have the Protestants obtained? Hopeless disunity and the destruction of Church life 12:46 An Orthodox researcher summarizes the state of Lutheranism 13:44 On Protestant student missions to Russia 15:31 St. Hilarion's pain of heart of the chasm between Protestant “Christian” life and true Church life 16:28 Appeals to create and obtain a common religion, a “union” of religions under general, abstract theses 17:27 Many think the Orthodox teaching on the Church is too lofty and too despotic, but true love requires humility and this is a great burden to egotists 19:00 Those who reject and misunderstand the true teaching on the Church may even condemn those who are enthusiastic about the Church and Church life 21:37 Churchless Christianity is death 22:56 Many are positive toward Christian teaching and even call themselves Christian while disdaining the Church and Church life 25:26 Can the Church not excommunicate those who reject Her? 28:00 The reason the Church's right of excommunication from the Church was readily accepted in past times 29:58 It seems the Church is in great disorder, what are we to do? 31:14 Many today are asking, “Where is the Church?” 32:13 Without clear boundaries between the Church and what is outside the Church, those seeking the Church can easily become wanderers and not Orthodox Christians 34:15 Orthodox Christians are responsible for making bright and clear the light of the Church for those seeking Her 35:27 “Only one who has come to believe in the Church, …one who has felt a Church life within himself, he and only he is on the correct path.” 36:12 One only comes to realize the truth and power of the Church by experience, not scholarly research 37:28 Any talk of “reviving the Church” is nonsense to one who lives Church life, for the life of the Church is the Holy Spirit 38:33 Church life is fullness of Christ and we must treasure and preach the truth and beauty of Church life 39:46 “While believing in the Church, we constantly seem to pardon ourselves for the fact that we still believe in it.” 41:08 CONCLUSION - “Thus it must be considered as the most vital necessity of the present time to confess openly that indisputable truth that Christ created precisely the Church and that it is absurd to separate Christianity from the Church and to speak of some sort of Christianity apart from the Holy Orthodox Church of Christ.” 42:05 A parable about a bird in storm, the tree he finds in refuge in is the Church "Members of the Church are very guilty in that they fail to point the way clearly and they poorly illuminate with their examples the final point of arrival for those who are seeking. This point is not the abstract understanding of Christianity, but precisely the Church of the living God." --- Send in a voice message: https://anchor.fm/orthodox-wisdom/message

Grace, grace, grace -- when you hear that word, what is the first thing that comes to mind? Well, the grace I am speaking of is the grace of God. But, why is His 'grace' of the utmost importance? Better yet, why should it matter to me? That my friend is an excellent question. Hence, this podcast episode, titled This is GRACE.  So, before we go any further, take a moment to look back over your life. Mainly, think about the mistakes you made, whether intentional or unintentional. No doubt, some mistakes were small, whereas others were doozies. But God had grace for it all. Moreover, His grace is available even now.  2 Corinthians 12:9 English Standard Version says,  “But he said to me, “My grace is sufficient for you, for my power is made perfect in weakness.” Therefore, I will boast all the more gladly of my weaknesses, so that the power of Christ may rest upon me.”  Now, just in case, you are someone who is thinking, "I've never made a mistake because I don't make mistakes." Then let me stop you right there. Why? Because there was only one perfect person who lived this life perfectly. And that was Jesus Christ of Nazareth. In fact, it is because of Him that grace is readily available to all who would receive it.  Conclusion  Thus, if you want to know more about the wonderful grace of God, then this podcast episode is for you. Go ahead and use the player at the top of this blog post. Or subscribe and listen via your preferred podcast platform. Then get encouraged by joining Lady V and me in our discussion –   Scriptures Referenced in Episode Discussion  Ephesians 1:3-14 John 3:16 Romans 10:9-10 Ephesians 6:23-24  Receive your Free Gift of Salvation – The Gospel of Jesus Christ  Explanation  If you are reading this, it is not by chance. This is your time to receive the Gift of Salvation through Christ Jesus. Now, you may be wondering, "Why do I need that?" Oh, I'm so glad you asked. The Bible says, that because Adam ate fruit from the tree of the knowledge of good and evil -- he released sin into the world.  And ultimately, Adam's sin brought death and death spread to everyone. No doubt, you may be thinking, "Of course, everyone is going to die." But, my question to you is "Where will you spend eternity?" Because there is life after death. In fact, when you die you go to one of two places -- heaven or hell.  Also, it is important to understand that, Adam's sin also brought an eternity in hell. But for those who choose not to receive the free gift of eternal life. Thus, you must make that choice before you take your last breath.  Romans 5:17 New Living Translation says, “For the sin of this one man, Adam, caused death to rule over many. But even greater is God's wonderful grace and his gift of righteousness, for all who receive it will live in triumph over sin and death through this one man, Jesus Christ.”  To sum it all up, Romans 6:23 New Living Translation says,  “For the wages of sin is death, but the free gift of God is eternal life through Christ Jesus our Lord.”  So, if you are reading this, don't let another day go by without receiving this life-changing gift.  Scripture   Romans 10:8-10 New Living Translation says,  “8 …“The message is very close at hand; it is on your lips and in your heart.” And that message is the very message about faith that we preach:  9 If you openly declare that Jesus is Lord and believe in your heart that God raised him from the dead, you will be saved.  10 For it is by believing in your heart that you are made right with God, and it is by openly declaring your faith that you are saved.”  Salvation Prayer  Lord Jesus, I am a sinner, and I am sorry for my sins. I ask You to forgive me. I want to follow You, Jesus. Come into my heart, into my life, and be my Lord and Savior. I believe in my heart that God raised you from the dead. By faith, I receive You, Jesus Christ, as my Lord and Savior.  Listen to We R S.H.

Welcome to The Nonlinear Library, where we use Text-to-Speech software to convert the best writing from the Rationalist and EA communities into audio. This is: EAA is overinvesting in corporate welfare reforms, published by kato on January 6, 2022 on The Effective Altruism Forum. Thank you to James Ozden for feedback on this post. In this post I argue that corporate welfare reforms (CWRs) are relatively overinvested in by the EA side of the animal movement (which I'll refer to as “EAA” from here on). Specifically, I believe that while CWRs are good, and in fact one of the most promising approaches we have, our enamoration with them leads us to underinvest in other approaches in a way that is suboptimal. By corporate welfare reforms, I mean instances where an animal protection NGO lobbies a corporation to transition at least part of their purchasing of a particular animal “product” over to that same “product” but raised in less bad conditions. The most common examples of CWRs are cage-free commitments and the Better Chicken Commitment. The core claims: CWRs currently command a significant portion of EAA's resources. CWRs, while good, have serious limitations. A pluralistic movement is more likely to end factory farming, and our current investment level in CWRs is stifling the development and refinement of alternative approaches. Conclusion: Thus, EAA ought to either 1) grow the pot of funds to invest more in non-CWR approaches, or 2) transition some of its resources from CWRs to other approaches. Below I explain my evidence for each claim in greater detail, and conclude with suggesting what we ought to do about this argument. Claim 1: CWRs currently command a significant portion of EAA's resources. James Ozden recently calculated that the three major funders in EAA, OpenPhil, the EA Fund (EAF), and ACE, had spent an estimated 60% of their animal welfare grants in the past 2 years on CWRS. This seems like a lot, and I'll go on to argue it's probably too high a proportion. For what proportion of institutional EAA money ought to go to CWRs, see Implications below. There's one counterargument I want to address here: Even with this much money going to CWRs, there's still a ton of money in the animal rights (AR) movement beyond EAA that doesn't go to CWRs. For instance, PETA brought in $64M in donations in 2020, more than double what the three EAA funders distributed in that time, and it's safe to say that none of PETA's income went to fund CWRs. Perhaps then it makes sense for EAA to overinvest in CWRs because the other side of the AR movement is underinvesting in them, so it in a way evens out. I find this argument somewhat compelling, but there is also a somewhat compelling response: if we believe that the EAA side of the animal movement has certain skills that the rest of the AR movement somewhat lacks, such as using and responding to evidence, it may make sense to avoid over-relying on the rest of the AR movement. Claim 2: CWRs, while good, have serious limitations. It's first worth noting that as an approach to help animals, CWRs are pretty awesome: They are probably the most impactful and the most scalable approach the animal movement has found. The fact that the smart people at these EAA granting organizations invest so heavily in them is evidence of this, as is the fact that the percent of chickens in cage-free housing has gone from 6% to at least 28% since 2015. As far as I'm aware, no other approach can claim such an impressive shift. CWRs also seem to pave the way for impressive legislative reforms, such as the European Commission's recent historic pledge to ban almost all cages and crates for farmed animals. But CWRs, like any approach, also have their limitations: Enforcement is not a given: A victory is not truly a victory until it is implemented and enforced. With cage-free, groups seem to have done well with enforcement. For other campaigns, including the Better Chicken Commitment, I'm less clear how well enforcem...

We pray through Hebrews 10:11-18. We use prayers also from Drawing near the throne: prayers by Berenice Aguilera

Objective: The metabolic syndrome, a major cluster of risk factors for cardiovascular diseases, shows increasing prevalence worldwide. Several studies have established associations of both apolipoprotein A5 (APOA5) gene variants and upstream stimulatory factor 1 (USF1) gene variants with blood lipid levels and metabolic syndrome. USF1 is a transcription factor for APOA5. Methods: We investigated a possible interaction between these two genes on the risk for the metabolic syndrome, using data from the German population-based KORA survey 4 (1,622 men and women aged 55-74 years). Seven APOA5 single nucleotide polymorphisms (SNPs) were analyzed in combination with six USF1 SNPs, applying logistic regression in an additive model adjusting for age and sex and the definition for metabolic syndrome from the National Cholesterol Education Program's Adult Treatment Panel III (NCEP (AIII)) including medication. Results: The overall prevalence for metabolic syndrome was 41%. Two SNP combinations showed a nominal gene-gene interaction (p values 0.024 and 0.047). The effect of one SNP was modified by the other SNP, with a lower risk for the metabolic syndrome with odds ratios (ORs) between 0.33 (95% CI = 0.13-0.83) and 0.40 (95% CI = 0.15-1.12) when the other SNP was homozygous for the minor allele. Nevertheless, none of the associations remained significant after correction for multiple testing. Conclusion: Thus, there is an indication of an interaction between APOA5 and USF1 on the risk for metabolic syndrome.

Background: Clinical chemical blood analysis including plasma electrolytes is routinely carried out for the diagnosis of various organ diseases. Phenotype-driven N-ethyl-N-nitrosourea (ENU) mouse mutagenesis projects used plasma electrolytes as parameters for the generation of novel animal models for human diseases. Methods: Here, we retrospectively evaluated the use of the plasma electrolytes calcium, chloride, inorganic phosphorus, potassium and sodium in the Munich ENU mouse mutagenesis project where clinical chemical blood analysis was carried out on more than 20,000 G1 and G3 offspring of chemically mutagenized inbred C3H mice to detect dominant and recessive mutations leading to deviations in various plasma parameter levels. Results: We identified a small number of animals consistently exhibiting altered plasma electrolyte values. Transmission of the phenotypic deviations to the subsequent generations led to the successful establishment of mutant lines for the parameters calcium and potassium. Published data from other phenotype-driven ENU projects also included only a small number of mutant lines which were generated according to altered plasma electrolyte levels. Conclusion: Thus, use of plasma electrolytes detected few mouse mutants in ENU projects compared to other clinical chemical blood parameters.

Background: Given the considerable toxicity and modest benefit of adjuvant chemotherapy for non-small cell lung cancer (NSCLC), there is clearly a need for new treatment modalities in the adjuvant setting. Active specific immunotherapy may represent such an option. However, clinical responses have been rare so far. Manipulating the host by inducing lymphopenia before vaccination resulted in a magnification of the immune response in the preclinical setting. To evaluate feasibility and safety of an irradiated, autologous tumor cell vaccine given following induction of lymphopenia by chemotherapy and reinfusion of autologous peripheral blood mononuclear cells (PBMC), we are currently conducting a pilot-phase I clinical trial in patients with NSCLC following surgical resection. This paper reports on the first clinical experience and evidence of an immune response in patients suffering from NSCLC. Methods: NSCLC patients stages I-IIIA are recruited. Vaccines are generated from their resected lung specimens. Patients undergo leukapheresis to harvest their PBMC prior to or following the surgical procedure. Furthermore, patients receive preparative chemotherapy ( cyclophosphamide 350 mg/m(2) and fludarabine 20 mg/m(2) on 3 consecutive days) for induction of lymphopenia followed by reconstitution with their autologous PBMC. Vaccines are administered intradermally on day 1 following reconstitution and every two weeks for a total of up to five vaccinations. Granulocytemacrophagecolony- stimulating-factor (GM-CSF) is given continuously ( at a rate of 50 mu g/24 h) at the site of vaccination via minipump for six consecutive days after each vaccination. Results: To date, vaccines were successfully manufactured for 4 of 4 patients. The most common toxicities were local injection-site reactions and mild constitutional symptoms. Immune responses to chemotherapy, reconstitution and vaccination are measured by vaccine site and delayed type hypersensitivity (DTH) skin reactions. One patient developed positive DTH skin tests so far. Immunohistochemical assessment of punch biopsies taken at the local vaccine site reaction revealed a dense lymphocyte infiltrate. Further immunohistochemical differentiation showed that CD1a+ cells had been attracted to the vaccine site as well as predominantly CD4+ lymphocytes. The 3-day combination chemotherapy consisting of cyclophosphamide and fludarabine induced a profound lymphopenia in all patients. Sequential FACS analysis revealed that different T cell subsets (CD4, CD8, CD4CD25) as well as granulocytes, B cells and NK cells were significantly reduced. Here, we report on clinical safety and feasibility of this vaccination approach during lymphoid recovery and demonstrate a patient example. Conclusion: Thus far, all vaccines were well tolerated. The overall trial design seems safe and feasible. Vaccine site reactions associated with infusion of GM-CSF via mini-pump are consistent with the postulated mechanism of action. More detailed immune-monitoring is required to evaluate a potential systemic immune response. Further studies to exploit homeostasis-driven T cell proliferation for the induction of a specific anti-tumor immune response in this clinical setting are warranted.

Background/Aim: Phenotype-driven screening of a great pool of randomly mutant mice and subsequent selection of animals showing symptoms equivalent to human kidney diseases may result in the generation of novel suitable models for the study of the pathomechanisms and the identification of genes involved in kidney dysfunction. Methods: We carried out a large-scale analysis of ethylnitrosourea (ENU)-induced mouse mutants for albuminuria by using qualitative SDS-polyacrylamide gel electrophoresis. Results: The primary albuminuria screen preceded the comprehensive phenotypic mutation analysis in a part of the mice of the Munich ENU project to avoid loss of mutant animals as a consequence of prolonged suffering from severe nephropathy. The primary screen detected six confirmed phenotypic variants in 2,011 G1 animals screened for dominant mutations and no variant in 48 G3 pedigrees screened for recessive mutations. Further breeding experiments resulted in two lines showing a low phenotypic penetrance of albuminuria. The secondary albuminuria screen was carried out in mutant lines which were established in the Munich ENU project without preceding primary albuminuria analysis. Two lines showing increased plasma urea levels were chosen to clarify if severe kidney lesions are involved in the abnormal phenotype. This analysis revealed severe albuminuria in mice which are affected by a recessive mutation leading to increased plasma urea and cholesterol levels. Conclusion: Thus, the phenotypic selection of ENU-induced mutants according to the parameter proteinuria in principle demonstrates the feasibility to identify nephropathy phenotypes in ENU-mutagenized mice. Copyright (C) 2005 S. Karger AG, Basel.