The Life of Jesus Outline Study

https://digitalcommons.acu.edu/crs_books/1444/thumbnail.jp

Spiritual Depression

https://digitalcommons.acu.edu/crs_books/1321/thumbnail.jp

1942: Abilene Christian College Bible Lectures - Full Text

Delivered in the Auditorium of Abilene Christian College, February, 1942 Abilene, Texas Published September, 1942 Price: $1.00. FIRM FOUNDATION PUBLISHING HOUSE Austin, Texa

1943: Abilene Christian College Bible Lectures - Full Text

Delivered in the Auditorium of Abilene Christian College February, 1943 Price: $1.00 FIRM FOUNDATION PUBLISHING HOUSE Austin, Texas Copyright, 1943 By Firm Foundation Publishing House Austin, Texa

1938: Abilene Christian College Bible Lectures - Full Text

Delivered in the Auditorium of Abilene Christian College, February, 1938 Abilene, Texas. Published October, 1939 PRICE, $1.00 FIRM FOUNDATION PUBLISHING HOUSE Austin, Texas

1946: Abilene Christian College Bible Lectures - Full Text

Abilene Christian College Lectures - 1946 INTRODUCTION It has been our purpose at Abilene Christian College down through the years to provide in the Annual Bible Lectureship programs that which would be appropriate for the time and most useful to the students and to the Lectureship visitors. The general subject for the 1946 lectures is “Things That Cannot Be Shaken.” This subject was selected because one of the battles, if not the battle, which the church faces today is against those forces which would undermine the bases of gospel truth. Many denominational leaders, in one way or another, are denying even the fundamentals of fundamentals— God is, the Bible is God\u27s Revelation, Jesus Christ is the Son of God and The Kingdom Cannot Be Shaken. Many others, some without knowing what they do, are accepting false teachings and ideologies which, if allowed to run their course, will destroy all true religion. It is believed that the 1946 lectures and this edition of the lectures will help toward establishing in the hearts of men the truth of the important theses discussed. It was the purpose of those who arranged the program that the Lectureship should, also, hold up Christianity as a working, practical religion; hence, the meetings on “Work in New Fields” and “The Church at Work.” The attendance of this Lectureship was the largest in the history of these yearly meetings. On Wednesday evening Brother Nichol spoke to a crowd of approximately 1700 persons. Other evening lectures were attended by crowds almost as large. Visitors came from more than a score of States and, also, from Canada and Mexico. It is the hope of all of us at the College that the fellowship of the 1946 Lectureship and the instruction given by the various speakers will continue to do good for years without end. DON H. MORRIS

1936: Abilene Christian College Bible Lectures - Full Text

Delivered in the auditorium of Abilene Christian College, Abilene, Texas, February 193

Common genetic variants in the CLDN2 and PRSS1-PRSS2 loci alter risk for alcohol-related and sporadic pancreatitis

Pancreatitis is a complex, progressively destructive inflammatory disorder. Alcohol was long thought to be the primary causative agent, but genetic contributions have been of interest since the discovery that rare PRSS1, CFTR, and SPINK1 variants were associated with pancreatitis risk. We now report two significant genome-wide associations identified and replicated at PRSS1-PRSS2 (1×10-12) and x-linked CLDN2 (p < 1×10-21) through a two-stage genome-wide study (Stage 1, 676 cases and 4507 controls; Stage 2, 910 cases and 4170 controls). The PRSS1 variant affects susceptibility by altering expression of the primary trypsinogen gene. The CLDN2 risk allele is associated with atypical localization of claudin-2 in pancreatic acinar cells. The homozygous (or hemizygous male) CLDN2 genotype confers the greatest risk, and its alleles interact with alcohol consumption to amplify risk. These results could partially explain the high frequency of alcohol-related pancreatitis in men – male hemizygous frequency is 0.26, female homozygote is 0.07

Rare coding variants in PLCG2, ABI3, and TREM2 implicate microglial-mediated innate immunity in Alzheimer's disease

We identified rare coding variants associated with Alzheimer’s disease (AD) in a 3-stage case-control study of 85,133 subjects. In stage 1, 34,174 samples were genotyped using a whole-exome microarray. In stage 2, we tested associated variants (P<1×10-4) in 35,962 independent samples using de novo genotyping and imputed genotypes. In stage 3, an additional 14,997 samples were used to test the most significant stage 2 associations (P<5×10-8) using imputed genotypes. We observed 3 novel genome-wide significant (GWS) AD associated non-synonymous variants; a protective variant in PLCG2 (rs72824905/p.P522R, P=5.38×10-10, OR=0.68, MAFcases=0.0059, MAFcontrols=0.0093), a risk variant in ABI3 (rs616338/p.S209F, P=4.56×10-10, OR=1.43, MAFcases=0.011, MAFcontrols=0.008), and a novel GWS variant in TREM2 (rs143332484/p.R62H, P=1.55×10-14, OR=1.67, MAFcases=0.0143, MAFcontrols=0.0089), a known AD susceptibility gene. These protein-coding changes are in genes highly expressed in microglia and highlight an immune-related protein-protein interaction network enriched for previously identified AD risk genes. These genetic findings provide additional evidence that the microglia-mediated innate immune response contributes directly to AD development