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Over the past two years, physician-scientist trainees have persevered in the face of evolving challenges presented by the ongoing coronavirus disease 2019 (COVID-19) pandemic. Research and healthcare institutions across the country continue to feel the impacts of the public health emergency. As scientists and physicians generate evidence to inform the prevention and treatment of COVID-19, physician-scientist trainees in all disciplines have adapted to the changing conditions of their education.

The 2020 Annual General Meeting (AGM) and Young Investigators’ Forum of the Canadian Society for Clinical Investigation / Société Canadienne de Recherches Clinique (CSCI/SCRC) and Clinician Investigator Trainee Association of Canada/Association des Cliniciens-Chercheurs en Formation du Canada (CITAC/ACCFC) was the first meeting to be hosted virtually. The theme was “Navigating Uncertainty, Embracing Change and Empowering the Next Generation of Clinician-Scientists”, and the meeting featured lectures and workshops that were designed to provide knowledge and skills for professional development of clinician investigator trainees. The opening remarks were given by Jason Berman (President of CSCI/SCRC), Tina Marvasti (President of CITAC/ACCFC) and Nicola Jones (University of Toronto Clinician Investigator Program Symposium Chair). Dr. Michael Strong, President of the Canadian Institutes of Health Research, delivered the keynote presentation titled “CIHR’s COVID-19 Response and Strategic Planning”. Dr. John Bell (University of Ottawa) received the CSCI Distinguished Scientist Award, Dr. Stanley Nattel (Université de Montréal) received the CSCI-RCPSC Henry Friesen Award (RCPSC; Royal College of Physicians and Surgeons of Canada) and Dr. Meghan Azad (University of Manitoba) received the CSCI Joe Doupe Young Investigator Award. Each scientist delivered talks on their award-winning research. The interactive workshops were “Developing Strategies to Maintain Wellness”, “Understanding the Hidden Curriculum: Power and Privilege in Science and Medicine”, “Hiring a Clinician Scientist Trainee: What Leaders Are Looking For” and “COVID-19: A Case Study for Pivoting Your Research”. The AGM included presentations from clinician investigator trainees nationwide. Over 70 abstracts were showcased, most are summarized in this review, and six were selected for oral presentations.

I hope you’re taking care and found some time to relax this summer. A new semester may mean a big transition—some folks are starting their graduate studies, re-entering clerkship, starting residency or entering a fellowship. For some, there will be little or no change at all; but just a continuation of one of the many phases of the physician-scientist training pathway. Whatever stage you’re at, the Clinical Investigator Trainee Association of Canada (CITAC) community is here to support and advocate for you!

The 2019 Annual General Meeting and Young Investigators’ Forum of the Canadian Society for Clinical Investigation / Société Canadienne de Recherche Clinique (CSCI/SCRC) and Clinician Investigator Trainee Association of Canada / Association des Cliniciens-Chercheurs en Formation du Canada (CITAC/ACCFC) was held in Banff, Alberta on November 8–10th, 2019. The theme was “Positioning Early Career Investigators for Success: Strategy and Resilience”. Lectures and workshops provided knowledge and tools to facilitate the attendees’ development as clinician investigators. Dr. Jason Berman (President of CSCI/SCRC), Elina Cook (President of CITAC/ACCFC) and Drs. Doreen Rabi and Zelma Kiss (University of Calgary Organizing Co-Chairs) gave opening presentations. The keynote speakers were Dr. William Foulkes (McGill University) (Distinguished Scientist Award winner) and Dr. Andrés Finzi (Université de Montréal) (Joe Doupe Young Investigator Award winner). Dr. Robert Bortolussi (Dalhousie University) received the Distinguished Service Award for his work as the Editor-in-Chief of Clinical and Investigative Medicine and for being instrumental in the development of the Canadian Child Health Clinician Scientist Program. This meeting was the first to host a panel discussion with Drs. Stephen Robbins and Marcello Tonelli from the Canadian Institutes of Health Research. Workshops on communication, career planning and work-life balance were hosted by André Picard and Drs. Todd Anderson, Karen Tang, William Ghali, May Lynn Quan, Alicia Polachek and Shannon Ruzycki. The AGM showcased 90 presentations from clinician investigator trainees from across Canada. Most of the abstracts are summarized in this review. Eight outstanding abstracts were selected for oral presentation at the President’s Forum.

It is important to strengthen critical thinking and scientific writing abilities during medical training to support trainees in their research endeavors and prepare students for careers in academic medicine. This commentary describes an interactive workshop to encourage student engagement with scientific literature and contribution to scholarly discourse by writing letters to the editor (LTEs). Students in the MD-PhD program at McGill University were asked to identify an article from a high-impact journal and think about ways in which they could address its scientific content. Students completed this preparation on their own time and then attended a 90-minute workshop where their LTEs were finalized and submitted. The LTE workshops were conducted in 2017 and 2019, and student participation and informal feedback indicated that perceptions of the workshops were positive. The workshops provided students an opportunity to strengthen their critical appraisal and academic communication skills while also contributing to the scientific literature. Letters written by aspiring and practicing physicians add valuable clinical insight to the literature and promote physician engagement with research. Strategies to support the adoption of LTE workshops include incorporating them into longitudinal curricula in medical school and integrating them into journal clubs during residency or fellowship.

People with Down syndrome (DS), caused by trisomy of chromosome 21 have a greatly increased risk of developing Alzheimer’s disease (AD). This is in part because of triplication of a chromosome 21 gene, APP. This gene encodes amyloid precursor protein, which is cleaved to form amyloid-β that accumulates in the brains of people who have AD. Recent experimental results demonstrate that a gene or genes on chromosome 21, other than APP, when triplicated significantly accelerate amyloid-β pathology in a transgenic mouse model of amyloid-β deposition. Multiple lines of evidence indicate that cysteine cathepsin activity influences APP cleavage and amyloid-β accumulation. Located on human chromosome 21 (Hsa21) is an endogenous inhibitor of cathepsin proteases, CYSTATIN B (CSTB) which is proposed to regulate cysteine cathepsin activity in vivo. Here we determined if three copies of the mouse gene Cstb is sufficient to modulate amyloid-β accumulation and cathepsin activity in a transgenic APP mouse model. Duplication of Cstb resulted in an increase in transcriptional and translational levels of Cstb in the mouse cortex but had no effect on the deposition of insoluble amyloid-β plaques or the levels of soluble or insoluble amyloid-β42, amyloid-β40, or amyloid-β38 in 6-month old mice. In addition, the increased CSTB did not alter the activity of cathepsin B enzyme in the cortex of 3-month or 6-month old mice. These results indicate that the single-gene duplication of Cstb is insufficient to elicit a disease-modifying phenotype in the dupCstb x tgAPP mice, underscoring the complexity of the genetic basis of AD-DS and the importance of multiple gene interactions in disease.

Individuals who have Down syndrome (caused by trisomy of chromosome 21), have a greatly elevated risk of early-onset Alzheimer’s disease, in which amyloid-β accumulates in the brain. Amyloid-β is a product of the chromosome 21 gene APP (amyloid precursor protein) and the extra copy or ‘dose’ of APP is thought to be the cause of this early-onset Alzheimer’s disease. However, other chromosome 21 genes likely modulate disease when in three-copies in people with Down syndrome. Here we show that an extra copy of chromosome 21 genes, other than APP, influences APP/Aβ biology. We crossed Down syndrome mouse models with partial trisomies, to an APP transgenic model and found that extra copies of subgroups of chromosome 21 gene(s) modulate amyloid-β aggregation and APP transgene-associated mortality, independently of changing amyloid precursor protein abundance. Thus, genes on chromosome 21, other than APP, likely modulate Alzheimer’s disease in people who have Down syndrome.

The Clinician Investigator Trainee Association of Canada (CI) trainees across the country around the common goal of improving training conditions for those pursuing a career at the junction of research and medicine. Since then, the CI training landscape has shifted dramatically. The number of Canadian CI trainees enrolled totaling 289 MD-PhD trainees and 389 Clinical Investigator Program (CIP) trainees as of 2019 [1]. Alumni outcome data have presented conclusive evidence that MD-PhD training programs are effective in producing CI careers [2–4].

People with Down syndrome (DS), caused by trisomy of chromosome 21 have a greatly increased risk of developing Alzheimer’s disease (AD). This is in part because of triplication of a chromosome 21 gene,APP. This gene encodes amyloid precursor protein, which is cleaved to form amyloid-β that accumulates in the brains of people who have AD. Recent experimental results demonstrate that a gene or genes on chromosome 21, other thanAPP,when triplicated significantly accelerate amyloid pathology in a transgenic mouse model of amyloid-β deposition. Multiple lines of evidence indicate that cysteine cathepsin activity influences APP cleavage and amyloid-β accumulation. Located on human chromosome 21 (Hsa21) is an endogenous inhibitor of cathepsin proteases,CYSTATIN B(CSTB)which is proposed to regulate cysteine cathepsin activityin vivo. Here we determined if three copies of the mouse geneCstbis sufficient to modulate beta amyloid (Aβ) accumulation and cathepsin activity in a transgenicAPPmouse model. Duplication ofCstbresulted in an increase in transcriptional and translational levels ofCstbin the mouse cortex but had no effect on the deposition of insoluble Aβ plaques or the levels of soluble or insoluble Aβ42, Aβ40, or Aβ38in 6-month old mice. In addition, the increased CSTB did not alter the activity of cathepsin B enzyme in the cortex of 3-month old mice. These results indicate that the single-gene duplication ofCstbis insufficient to elicit a disease-modifying phenotype in the dupCstb x tgAPP mice, underscoring the complexity of the genetic basis of AD-DS and the importance of multiple gene interactions in disease.

Tetraarylmethanes are an important class of molecules that contain four aryl groups bonded to a central carbon atom. The shape/three-dimensionality of these molecules makes them suitable for organic light-emitting diodes (OLEDs), organic solar cells, hydrogen storage, and even drug-delivery. Despite their importance, there are only a few methods available for their preparation. Herein, we report a simple procedure for the preparation of tetraarylmethanes that involves a bismuth-catalyzed Friedel-Crafts cyclization followed by a desulfurization reaction mediated by Raney nickel.

Alzheimer’s disease (AD) pathology causes microstructural changes in the brain. These changes, if quantified with magnetic resonance imaging (MRI), could be studied for use as an early biomarker for AD. The aim of our study was to determine if T(1) relaxation, diffusion tensor imaging (DTI), and quantitative magnetization transfer imaging (qMTI) metrics could reveal changes within the hippocampus and surrounding white matter structures in ex vivo transgenic mouse brains overexpressing human amyloid precursor protein with the Swedish mutation. Delineation of hippocampal cell layers using DTI color maps allows more detailed analysis of T(1)-weighted imaging, DTI, and qMTI metrics, compared with segmentation of gross anatomy based on relaxation images, and with analysis of DTI or qMTI metrics alone. These alterations are observed in the absence of robust intracellular Aβ accumulation or plaque deposition as revealed by histology. This work demonstrates that multiparametric quantitative MRI methods are useful for characterizing changes within the hippocampal substructures and surrounding white matter tracts of mouse models of AD.

Strain sensors (e.g., fiber optic strain sensors) can be used to measure the deformation of flexible rockets during launches, in order to monitor and control rocket flight attitude. In this paper, strain sensors are instrumented on multi-axial reference strain structures for a convenient monitor of rocket bending vibrations. Reference strain structures are attached longitudinally along the outer surface of thin-walled flexible rockets. As the medium between the sensors and rocket, the structural design of reference strain structures, as well as the sensor spacing along them, is optimized using an integrated multi-objective optimization approach, which ensures that the reference strain structures will accurately track the deformation of the rocket surface. In addition, kinematic equations are developed to allow for an accurate prediction of the bending deflection of the rocket center axis by using the strain data measured on the rocket surface. Finally, the performance of the optimal reference strain structure is evaluated using different numerical simulations of the flexible rocket.

Very low frequency communication systems (3 kHz–30 kHz) enable applications not feasible at higher frequencies. However, the highest radiation efficiency antennas require size at the scale of the wavelength (here, >1 km), making portable transmitters extremely challenging. Facilitating transmitters at the 10 cm scale, we demonstrate an ultra-low loss lithium niobate piezoelectric electric dipole driven at acoustic resonance that radiates with greater than 300x higher efficiency compared to the previous state of the art at a comparable electrical size. A piezoelectric radiating element eliminates the need for large impedance matching networks as it self-resonates at the acoustic wavelength. Temporal modulation of this resonance demonstrates a device bandwidth greater than 83x beyond the conventional Bode-Fano limit, thus increasing the transmitter bitrate while still minimizing losses. These results will open new applications for portable, electrically small antennas., Designing high radiation efficiency antennas for portable transmitters in low frequency communication systems remains a challenge. Here, the authors report on using piezoelectricity to more efficiently radiate while achieving a bandwidth eighty three times higher than the passive Bode-Fano limit.

This paper presents results from tests aimed to assess the relative ductility of titanium alloy Ti 6Al-4V and stainless steel A286 aerospace fasteners of comparable size and tensile strength. A test procedure is developed, and tensile tests are performed on test fasteners. All test fasteners fracture in the threaded region. Elastic and plastic deformation at rupture are extracted from the resulting load versus displacement curves and used to compute the ductility index for each test fastener. The ductility index quantifies the relative ductility between the different fastener materials. The average ductility index for the titanium alloy fasteners is about one-tenth the average value for the A286 fasteners. In addition, the fracture surfaces of the titanium alloy test fasteners fracture perpendicular to the axis of tensile loading, whereas the A286 test fasteners fracture across three or four threads, which corresponds to about a 45° angle. Both the relative ductility index values and fracture surface characteristics indicate much less ductility in the titanium alloy fasteners. These results are not intended to discourage the use of titanium alloy fasteners but rather to provide additional data for use in proper joint design when the benefits of lower weight or extreme temperature use are required.

Down syndrome, caused by trisomy of chromosome 21, is the single most common risk factor for early-onset Alzheimer's disease. Worldwide approximately 6 million people have Down syndrome, and all these individuals will develop the hallmark amyloid plaques and neurofibrillary tangles of Alzheimer's disease by the age of 40 and the vast majority will go on to develop dementia. Triplication of APP, a gene on chromosome 21, is sufficient to cause early-onset Alzheimer's disease in the absence of Down syndrome. However, whether triplication of other chromosome 21 genes influences disease pathogenesis in the context of Down syndrome is unclear. Here we show, in a mouse model, that triplication of chromosome 21 genes other than APP increases amyloid-β aggregation, deposition of amyloid-β plaques and worsens associated cognitive deficits. This indicates that triplication of chromosome 21 genes other than APP is likely to have an important role to play in Alzheimer's disease pathogenesis in individuals who have Down syndrome. We go on to show that the effect of trisomy of chromosome 21 on amyloid-β aggregation correlates with an unexpected shift in soluble amyloid-β 40/42 ratio. This alteration in amyloid-β isoform ratio occurs independently of a change in the carboxypeptidase activity of the γ-secretase complex, which cleaves the peptide from APP, or the rate of extracellular clearance of amyloid-β. These new mechanistic insights into the role of triplication of genes on chromosome 21, other than APP, in the development of Alzheimer's disease in individuals who have Down syndrome may have implications for the treatment of this common cause of neurodegeneration.

Background Talactoferrin alfa is an oral dendritic cell (DC)-mediated immunotherapy (DCMI). We tested whether talactoferrin was superior to placebo in advanced non-small-cell lung cancer (NSCLC). Patients and methods An FORTIS-M trial was an international, multicenter, randomized, double-blind comparison of talactoferrin (1.5g p.o. BID) versus placebo BID, in patients with stage IIIB/IV NSCLC whose disease had failed two or more prior regimens. Treatment was administered for a maximum of five 14-week cycles. The primary efficacy end point was overall survival (OS); secondary end points included 6- and 12-month survival, progression-free survival (PFS), and disease control rate (DCR). Results Seven hundred and forty-two patients were randomly assigned (2:1) to talactoferrin (497) or placebo (245). The median OS in the intent-to-treat (ITT) population was 7.66 months in the placebo arm and 7.49 months in the talactoferrin arm [hazard ratio (HR), 1.04; 95% CI, 0.873–1.24; P = 0.6602]. The 6-month survival rates were 59.9% (95% CI, 53.4% to 65.8%) and 55.7% (95% CI, 51.1% to 59.9%), respectively. The 12-month survival rates were 32.2% (95% CI, 26.3% to 38.2%) and 30.9% (95% CI, 26.8% to 35%), respectively. The median PFS rates were 1.64 months and 1.68 months, respectively (HR, 0.99; 95% CI, 0.835–1.16; P = 0.8073). The DCRs were 38.4 and 37.6%, respectively [stratified odds ratio (OR), 0.96; 95% CI, 0.698–1.33; P = 0.8336]. The safety profiles were comparable between arms. Conclusions There was no improvement in efficacy with talactoferrin alfa in patients with advanced NSCLC whose disease had failed two or more previous regimens.

Pregnenolone sulfate (PS) is a neuroactive steroid that directly modulates glutamate and GABAA receptor function, suggesting that it may regulate the balance between excitatory and inhibitory neurotransmission (Farb and Gibbs 1996; Gibbs and Farb 2000). PS also modulates the activity of AMPA and kainate receptors (Wu et al. 1991), σ receptors (Monnet et al. 1995; Hayashi et al. 2000), and certain voltage-gated calcium channels (Bukusoglu and Sarlak 1996; Hige et al. 2006). Modulation of synaptic transmission by PS has been demonstrated in multiple experimental paradigms. PS potentiates spontaneously occurring excitatory postsynaptic currents (EPSCs) in hippocampal cell cultures (Park-Chung et al. 1997; Meyer et al. 2002) and in slices prepared from rat pre-limbic cortex (Dong et al. 2005), as well as evoked EPSCs from hippocampal (Schiess et al. 2006) and calyx of Held synapses (Hige et al. 2006). PS also augments NMDAR independent long term potentiation in the rat hippocampus via modulation of L-type Ca2+ channels and σ receptors (Sabeti et al. 2007), and a PS-like retrograde modulatory factor plays a role in plasticity of immature hippocampal synapses (Mameli et al. 2005). Enzymes for synthesis of pregnenolone from cholesterol (cytochrome P450 scc) and sulfation of pregnenolone to PS (neurosteroid sulfotransferase ST2A1, SULT2B1a) are present in neural tissue (Hojo et al. 2004; Kohjitani et al. 2006). Pregnenolone is inactive at both glutamate and GABAA receptors, indicating that the negatively charged sulfate group of PS is essential for its modulatory activity. Whereas pregnenolone is neutral and lipophilic, permitting rapid permeation across cell membranes, sulfation to form PS results in a negatively charged steroid that could be compartmentalized intracellularly. Pregnenolone sulfotransferase is present in rat C6 glioma cells, where its activity is regulated by AMPA receptors (Kohjitani et al. 2008). Steroid sulfatases are present in rodent, bovine, monkey, and human brain and offer a potential mechanism for inactivation of PS (Compagnone et al. 1997; Mellon et al. 2001; Plassart-Schiess and Baulieu 2001). Collectively, these observations indicate that PS satisfies several classical criteria for identification as a neurotransmitter or neuromodulator: it is synthesized in nervous tissue, has specific receptor pharmacology, and is inactivated by removal of the sulfate group, but the role of PS within the nervous system remains unresolved. Whether PS is stored and released at physiologically active concentrations by either neurons or glia has remained a controversial issue. The average tissue level of PS in extracts of postmortem aged human brain was found to be 2.8 nM in frontal cortex and 4.6 nM in cerebellum, while blood plasma contains about 380 nM free sulfated steroid. In rat, however, the average level of PS in adrenal tissue was 14 nM but was only 0.64 nM in two of five samples from anterior brain (limit of detection: 0.38 nM) and undetectable in other brain regions (Liere et al. 2004). Another study (Ebner et al. 2006) failed to detect PS in extracts of pooled whole rat brain, with a reported detection limit of 141 pM. Nevertheless, the inability to detect gross tissue levels of PS in various regions of rat brain does not exclude the possibility that significant amounts of this steroid might be present on a cellular level (Schumacher et al. 2008). Infusion of 10 nM PS into rat striatum via reverse microdialysis results in a significant increase in dopamine (DA) overflow in the striatum that involves NMDA receptor (NMDAR) function, but not σ receptor function (Sadri-Vakili et al. 2008; Gibbs et al. 2006). To ask whether this high affinity effect of PS was exerted via modulation of presynaptic NMDARs located on dopaminergic terminals, we investigated the effect of PS on DA release ex vivo from a preparation of striatal nerve terminals comprised of mixed synaptosomes and synaptoneurosomes (SSNs). We report that PS at concentrations as low as 25 pM induces [3H]DA release from striatal SSNs, while pregnenolone is without effect, suggesting that subnanomolar concentrations of PS could modulate nigro-striatal DA release. To our knowledge, this study is the first to report direct neurosteroid enhancement of NMDAR-dependent synaptosomal transmitter release at subnanomolar concentrations of steroid.

Infrared transmission measurements of Bridgman grown AgGaSe 2 chalcopyrite show a deleterious absorption peak centered at 9.3 μm. The 9.3 μm absorption was reduced by 63% using an additional post-growth heat treatment at 790 °C in a controlled partial pressure of selenium of 0.243 atm for 4000 min. A linear correlation was determined between infrared absorption and the selenium partial pressure during the heat treatments: α 9.3 μm =−0.4048( P Se ) atm −1 cm −1 +0.1322 cm −1 . A linear correlation was also determined between dark resistivity and 9.3 μm absorption coefficient: ρ =−7×10 12 α 9.3 μm Ω cm 2 +1×10 12 Ω cm. This correlation indicates that stoichiometric AgGaSe 2 should have a dark resistivity of 10 12 Ω cm. These results support the identification of the 9.3 μm absorption defect as a native selenium vacancy.

SUMMARYThis paper investigates vehicle dynamics and control from a systems theoretic perspective. Based on improved understanding of MIMO vehicle systems, a four-wheel-steering robust model following control strategy including a virtual vehicle model, a feed-forward internal model and a feedback element is proposed for improving the dynamic performance of the vehicle. The controller gain matrices are determined by a joint eigenstructure assignment and mixed-sensitivity H∞ control technique to satisfy both time- and frequency-domain specifications. The purpose is to improve disturbance rejection performance at low frequencies as well as to enhance robust stability against unstructured multiplicative output perturbations at high frequencies. The performance and robustness are assessed by numerical simulation.

Optic chiasm lesions in myelin oligodendrocyte glycoprotein (MOG)–experimental autoimmune encephalomyelitis (EAE) mice were characterized using magnetic resonance imaging (MRI) and validated using electron microscopy (EM). MR images were collected from 3 days after induction to remission, approximately 20 days after induction. Hematoxylin and eosin, solochrome cyanin–stained sections, and EM images were obtained from the optic chiasms of some mice approximately 4 days after disease onset when their scores were thought to be the highest. T2-weighted imaging and apparent diffusion coefficient map hyperintensities corresponded to abnormalities in the optic chiasms of EAE mice. Mixed inflammation was concentrated at the lateral surface. Degeneration of oligodendrocytes, myelin, and early axonal damage were also apparent. A marked increase in chiasm thickness was observed. T2-weighted and diffusion-weighted MRI can detect abnormalities in the optic chiasms of MOG-EAE mice. MRI is an important method in the study of this model toward understanding optic neuritis.

Thermally stimulated luminescence measurements on cerium-doped M 2 SiO 5 (M=Lu, Y, Yb, Er) and undoped Lu 2 SiO 5 , each possessing monoclinic C2/c crystal symmetry, reveal common glow peaks with the principal one occurring near 375 K. In contrast, cerium-doped Gd 2 SiO 5 , characterized by the monoclinic P2 1 /c structure, exhibits a different glow curve with the principal peak occurring near 425 K. Although undoped Lu 2 SiO 5 shares the characteristic Ce-doped M 2 SiO 5 glow curve, emission spectra data show that it emits weak line-emission, whereas the cerium-doped materials are characterized by the intense Ce 3+ band spectrum. This suggests a common and unique trapping site whose formation does not require the presence of cerium. Application of peak-shape glow curve analysis shows that the characteristic peak near 375 K in each sample obeys first-order kinetics with thermal activation energy approx. 1 eV and frequency factor ∼10 14 s −1 . Based on these results, we suggest that the characteristic glow peak is intrinsic and independent of cerium doping. This unique defect is common to the C2/c-structured oxyorthosilicates and is related to the host metal–ion–ligand configuration.

Temperature-dependent optical absorption of cerium-doped gadolinium oxyorthosilicate (Gd2SiO5:Ce) has been measured and analyzed for impurity-ion-lattice coupling parameters and oscillator strengths. Although the spectrum consists of overlapping Ce3+ bands and Gd3+ lines, two well-resolved Ce3+ bands with 10 K maxima at 3.32 eV (peak a) and 3.61 eV (peak b) are amenable to spectral analysis. These bands, previously assigned to Ce3+ ions occupying crystallographically inequivalent substitutional sites, are characterized by Gaussian line shapes and temperature-dependent half widths that are well described by the linear model of impurity-ion-lattice coupling. Huang–Rhys [Proc. R. Soc. A 204, 404 (1950)] parameters of peaks a and b are 22.7 and 5.7, respectively, indicating strong ion-lattice coupling, with vibrational frequencies 1.83×1013 s−1 (peak a) and 5.07×1013 s−1 (peak b). Peak b centroid is approximately temperature independent, but peak a centroid shifts to higher energy with increasing temperature. This dependence is adequately described by including higher-order coupling terms in the ion-lattice interaction, although crystal-field contributions cannot be excluded. Absorption band oscillator strengths, f, are calculated from Smakula’s [Z. Phys. 59, 603 (1930)] formula and knowledge of cerium concentration for the two inequivalent sites. In the interval 10–300 K, peak a f values range from (9.8 to 26.8)×10−4 and peak b f values vary from (7.8 to 5.8)×10−3. From the known correlation between oscillator strength and metal-ion-ligand separation, we identify peaks a and b as the seven- and nine-oxygen-coordinated sites, respectively.