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The article presents the author's reply to comments in response to his article in favor of British writer C.S. Lewis' apologetic Trilemma argument for the deity of Jesus Christ. The author believes that Lewis' argument as presented in the book "Mere Christianity" assumes without argument that Jesus claims to be God. According to the author, the main point of disagreement seems to be over how strong the case for Jesus' claims to deity actually is.

The article presents the author's views in favor of British writer C.S. Lewis' apologetic Trilemma argument for the deity of Jesus Christ. The author mentions Lewis' argument mentioned in his book "Mere Christianity," in which he assumes that Jesus claimed to be God. According to the author, Lewis's tripartite form of Jesus gave birth to the Trilemma.

Background To characterize regional kidney sodium response by MRI following NKCC2 inhibition. Methods Regional renal sodium signals were monitored noninvasively using 23Na-MRI at 9.4T with a temporal resolution of 1.5 min in anesthetized rats (N = 14). A mild NKCC2 inhibition was induced using a slow intravenous furosemide infusion. Time course of sodium signal was modeled as an exponential transient with a single characteristic time constant. Results Under normal physiological conditions, the renal sodium signals in medullary and cortical regions were stable and found to respond differently to furosemide challenge. Furosemide infusion at 1.2 mg/kg/h (N = 7) increased sodium signal in the cortex by 40 ± 6% ( P < 7 × 10−5) whereas decreased in the medulla by 29 ± 2% ( P < 3 × 10−6) with different temporal kinetics. The characteristic time constants of the change were determined to be: 8 ± 2 and 70 ± 10 min for medulla and cortex. Also, the medullary change occurred 9(±3) times faster than cortical independent of furosemide infusion rate up to 35 mg/kg/h. Conclusion The pharmacological effects in terms of regional kidney sodium signal changes induced by NKCC2 inhibition are region-specific and highly predictable. Using noninvasive sodium MRI, we obtained regional renal sodium kinetics data sets in response to a low dose furosemide infusion in normal rats. J. Magn. Reson. Imaging 2015;41:1622-1628. © 2014 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Background: Pharmacological MRI (phMRI) is a neuroimaging technique where drug-induced hemodynamic responses can represent a pharmacodynamic biomarker to delineate underlying biological consequences of drug actions. In most preclinical studies, animals are anesthetized during image acquisition to minimize movement. However, it has been demonstrated anesthesia could attenuate basal neuronal activity, which can confound interpretation of drug-induced brain activation patterns. Significant efforts have been made to establish awake imaging in rodents and nonhuman primates (NHP). Whilst various platforms have been developed for imaging awake NHP, comparison and validation of phMRI data as translational biomarkers across species remain to be explored. Methodology: We have established an awake NHP imaging model that encompasses comprehensive acclimation procedures with a dedicated animal restrainer. Using a cerebral blood volume (CBV)-based phMRI approach, we have determined differential responses of brain activation elicited by the systemic administration of buprenorphine (0.03 mg/kg i.v.), a partial µ-opioid receptor agonist, in the same animal under awake and anesthetized conditions. Additionally, region-of-interest analyses were performed to determine regional drug-induced CBV time-course data and corresponding area-under-curve (AUC) values from brain areas with high density of µ-opioid receptors. Principal Findings: In awake NHPs, group-level analyses revealed buprenorphine significantly activated brain regions including, thalamus, striatum, frontal and cingulate cortices (paired t-test, versus saline vehicle, p<0.05, n = 4). This observation is strikingly consistent with µ-opioid receptor distribution depicted by [6-O-[11C]methyl]buprenorphine ([11C]BPN) positron emission tomography imaging study in baboons. Furthermore, our findings are consistent with previous buprenorphine phMRI studies in humans and conscious rats which collectively demonstrate the cross-species translatability of awake imaging. Conversely, no significant change in activated brain regions was found in the same animals imaged under the anesthetized condition. Conclusions: Our data highlight the utility and importance of awake NHP imaging as a translational imaging biomarker for drug research. [ABSTRACT FROM AUTHOR]

31P Nuclear magnetic resonance (NMR) spectroscopy and 1H NMR imaging were used to examine the effect of short-term ethanol feeding on the rat testis. Weanling rats were pair-fed for 10 weeks either on ethanol containing liquid diet (36% ethanol of total calories) or a diet in which dextrimaltose was isocalorically substituted for the ethanol of the alcohol-containing diet. In vivo 31P NMR of the testes was used to determine the intratesticular pH and the relative concentrations of various phosphorus-containing metabolites. The integrity of the blood-testes barrier was evaluated using 1H NMR imaging following a gadolinium diethylene tetramine pentacetic acid derlvative (Gd-DTPA) administration as a vascular contrast agent. After the completion of NMR studies, the testis and the liver were freezeclamped to allow for the assay of their adenosine-5′-triphosphate (ATP) contents. Serum was assayed for its content of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alcohol and testosterone. Ethanol feeding resulted in the following: (a) a reduction in the body weight (p < 0.05), (b) a reduction in the testicular phosphodiesters (PDE) PDE/ATP ratio ( p < 0.05), (c) an increased change in the testis image intensity difference between pre- and post-iv Gd-DTPA images, (c) a reduction in the testicular and hepatic content of ATP, and (d) increased serum levels of AST and ALT. Therefore, using NMR Spectroscopy and imaging, it has been possible to demonstrate that the metabolic alterations which occur in the testes in response to short-term ethanol feeding within the present experimental protocol precede the reduction in the serum testosterone level produced by ethanol and is associated with an early disruption of the blood testes barrier. [ABSTRACT FROM AUTHOR]