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For patients with borderline annulus areas that fall between two valve sizes, overinflating a smaller balloon-expandable transcatheter heart valve (THV) may be preferable to nominal sizing of a larger THV.To evaluate the outcomes of nominal preparation versus over-expanding an under-sized SAPIEN 3 Ultra (S3U) transcatheter heart valve (OE-THV) in cases with borderline annuli.958 patients that underwent TAVR with the S3U at four high-volume TAVR centers between January 2017 and December 2020 were retrospectively reviewed. 336 patients were identified as borderline annuli size, of which 146 (44%) received OE-THVs and 190 (56%) received nominal-sized THVs. The primary composite endpoint included: in-hospital mortality, aortic injury, moderate/severe paravalvular leak (PVL), permanent pacemaker implant (PPM), stroke, or conversion to surgery.Baseline characteristics were similar except for a larger percentage of females in the OE-THV (53.42% vs. 42.11%, p = 0.04). TAVR with OE-THV resulted a reduction in the primary composite endpoint (13.69% vs. 22.63%, p = 0.04). On subgroup analysis, there was no difference between 20 mm OE-THV versus 23 mm nominal or 23 mm OE-THV versus 26 mm nominal, but there was a reduction in the primary composite endpoint in patients with larger annuli that received a 26 mm OE-THV compared to the 29 mm nominally sized THV (9.7% vs. 27.4%, p = 0.02). At 1 month and 1 year follow-up, there was no significant difference in mortality, PVL rates, NYHA class, and/or KCCQ score.Overinflating a smaller-sized S3U THV may be a safer option in comparison to nominal sizing in patients with borderline annular area.

Prior studies suggest a strong genetic influence on breast cancer prognosis. Six genome-wide association studies (GWAS) on breast cancer prognosis have been published to date. However, none of the reported loci was replicated across studies and only two passed genome-wide significance (P < 5 x 10-8). In the Pathways Study, a prospective cohort of breast cancer survivors begun in Kaiser Permanente Northern California (KPNC) in 2006, we carried out a GWAS of overall survival (OS) in 3,973 patients. Trans-ethnic meta-GWAS identified an association with OS of a locus on chromosome 15 that almost reached genome-wide significance (P = 9.42 x 10-8). This locus spanned the UACA gene, a key regulator of tumor suppressor Par-4. We found that receipt of chemotherapy modified the effect of the UACA locus on OS (Pinteraction = 2.4 x 10-4). This observation led us to hypothesize that the UACA locus effect on OS may be specific to Par-4 dependent chemotherapies, which include anti-HER2 therapy and doxorubicin. We stratified patients into two groups, those who received Par-4 dependent chemotherapy agents versus other patients. In separate trans-ethnic meta-GWAS, the UACA locus was significantly associated with OS in patients taking Par-4 dependent chemotherapies (P = 1.27 x 10-9), while no association was observed in the other patients (P = 0.21). To evaluate whether the UACA gene may be responsible for this association, we performed a transcriptome-wide association study (TWAS) of OS in White patients taking Par-4 dependent chemotherapies. Higher UACA gene expression was significantly associated with OS (P = 4.68 x 10-7), the only gene reaching transcriptome-wide significance (P < 4.34 x 10-6). These results suggest that higher UACA expression may inhibit Par-4 induced apoptosis and lead to stronger chemoresistance and worse survival. We attempted to validate our findings in the independent KPNC Genetic Epidemiology Research on Aging (GERA) cohort. The GERA cohort included only 168 White patients with incident breast cancer after DNA collection who received Par-4 dependent chemotherapies. We found a non-significant association (hazard ratio (HR) = 1.46, P = 0.66) consistent with Pathways Study findings. However, the GERA cohort also included 1,983 prevalent breast cancer patients with biospecimen collection after diagnosis. In this group, the risk allele frequency in breast cancer survivors receiving Par-4 dependent chemotherapies was significantly lower than that in the White population (P = 5.50 x 10-3) while the risk allele frequency in the those not receiving these chemotherapies was similar to the population (P = 0.07). This is consistent with Pathways Study observations that the UACA locus risk allele significantly increased risk of mortality in patients taking Par-4 dependent chemotherapies. A higher mortality in breast cancer survivors carrying the risk allele would result in decreased risk allele frequency. We further validated our findings in Shanghai Breast Cancer Survival Study (SBCSS)and Shanghai Breast Cancer Study, which were conducted from 1996 to 2006 in urban Shanghai and recruited 5,575 breast cancer patients. In this independent Asian breast cancer population, the UACA locus was modestly associated with OS in the overall population (HR = 1.18, P = 0.012), and more significantly in 1,289 SBCSS patients who received anthracyclines (HR = 1.66, P = 1.55 x 10-4). This is the first human study suggesting the Par-4 pathway affects breast cancer patient survival with UACA a key modulator of treatment outcomes by anti-Her2 therapy and doxorubicin. Our findings suggest a path toward new predictive pharmacogenetic markers for personalized medicine targeting the Par-4 pathway for breast cancer treatment. Citation Format: Lawrence H Kushi, Qianqian Zhu, Emily Schultz, Jirong Long, Janise M Roh, Emily Valice, Cecile A Laurent, Li Yan, Isaac J Ergas, Warren Davis, Dilrini K Ranatunga, Marilyn L Kwan, Ping-Ping Bao, Wei Zheng, Xiao-Ou Shu, Christine B Ambrosone, Song Yao. Genome-wide association study identifies UACA as a modulator of breast cancer chemoresistance and survival [abstract]. In: Proceedings of the 2020 San Antonio Breast Cancer Virtual Symposium; 2020 Dec 8-11; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2021;81(4 Suppl):Abstract nr GS2-05.

Hispanic children have a higher incidence of acute lymphoblastic leukemia (ALL) and inferior treatment outcomes relative to non-Hispanic White children. We previously reported that Hispanic children with ALL had lower risk of fracture and osteonecrosis. To unravel the genetic root of such ethnic differences, we genotyped 449 patients from the DFCI 05-001 cohort and analyzed their ancestry. Patients with discordant clinical and genetic ancestral groups were reclassified, and those with unknown ancestry were reassigned on the basis of genetic estimates. Both clinical and genetic ancestries were analyzed in relation to risk of bone toxicities and survival outcomes. Consistent with clinically reported race/ethnicity, genetically defined Hispanic and Black patients had significantly lower risk of fracture (Hispanic: subdistribution hazard ratio [SHR], 0.42; 95% confidence interval [CI], 0.22-0.81; P = .01; Black: SHR, 0.28; 95% CI, 0.10-0.75; P = .01), and osteonecrosis (Hispanic: SHR, 0.12; 95% CI, 0.02-0.93; P = .04; Black: SHR, 0.24; 95% CI, 0.08-0.78; P = .02). The lower risk was driven by African but not Native American or Asian ancestry. In addition, patients with a higher percentage of Native American ancestry had significantly poorer overall survival and event-free survival. Our study revealed that the lower risk of bone toxicities among Black and Hispanic children treated for ALL was attributed, in part, to the percentage of African ancestry in their genetic admixture. The findings provide suggestive evidence for the protective effects of genetic factors associated with African decent against bone damage caused by ALL treatment and clues for future studies to identify underlying biological mechanisms.

While BRCA1 and BRCA2 mutations are known to confer the largest risk of breast cancer and ovarian cancer, the incomplete penetrance of the mutations and the substantial variability in age at cancer onset among carriers suggest additional factors modifying the risk of cancer in BRCA1/2 mutation carriers. To identify genetic modifiers of BRCA1/2, we carried out a whole-genome sequencing study of 66 ovarian cancer patients that were enriched with BRCA carriers, followed by validation using data from the Pan-Cancer Analysis of Whole Genomes Consortium. We found PPARGC1A, a master regulator of mitochondrial biogenesis and function, to be highly mutated in BRCA carriers, and patients with both PPARGC1A and BRCA1/2 mutations were diagnosed with breast or ovarian cancer at significantly younger ages, while the mutation status of each gene alone did not significantly associate with age of onset. Our study suggests PPARGC1A as a possible BRCA modifier gene. Upon further validation, this finding can help improve cancer risk prediction and provide personalized preventive care for BRCA carriers.

Ecologists have long sought to understand the controls of species’ geographic distributions. Two important hypotheses have been that range limits are determined 1) predominantly by climate or 2) by competition in addition to climate, with competitive interactions dominating where climate is benign. If the first hypothesis is correct, the effect of changing climate on species’ distributions should be adequately predicted by climate-only models. Here, we used demographic range models (DRMs) to evaluate the influence of climate and competition on the geographic distribution of Pinus edulis, a desert pine in the southwestern U.S. We parameterized DRMs with data on 23,426 trees in 1,941 forest inventory plots. Vital rate responses were consistent with the predictions of the second hypothesis: negative effects of warm-dry conditions at low-elevation sites and competition at cool-humid, high-elevation sites. Further, including both climate and competition in the DRM yielded a better fit of DRM-predicted population growth rate to the observed distribution than a climate-only DRM. However, at cool-humid sites, negative effects of competition were too weak to offset positive climate effects, resulting in a mismatch between predicted population growth rate and observed distribution. This result leads us to formulate a new hypothesis: climate has complex influences on species’ distributions through its effects on range-limiting processes at a variety of scales, for example, biotic and disturbance feedbacks at community, ecosystem, landscape, and macrosystem scales. The implications of this complex systems hypothesis are that range dynamics may be poorly predictable from static, climate-only models, and may be characterized by sudden changes in abundance, even distribution collapse, with climate change.

Background A study was initiated at Roswell Park Comprehensive Cancer Center to capture the real-world experience related to the use of CDK4/6 inhibitors (Ciclibs) for the treatment of metastatic hormone receptor-positive and HER2-negative breast cancer (HR+/HER2-). Patients and Methods A total of 222 patients were evaluated who received CDK4/6 inhibitors in the period from 2015 to 2021. Detailed clinical and demographic information was obtained on each patient and used to define clinical and demographic features associated with progression-free survival on CDK4/6 inhibitor-based therapies. Results In this real-world analysis, the majority of patients received palbociclib as the CDK4/6 inhibitor with letrozole or fulvestrant as the predominant endocrine therapies. The median progression-free survival (PFS) in the letrozole (27.6 months) and fulvestrant (17.2 months) groups were comparable to that observed in clinical trials. As expected, age at start of the treatment and menopausal status influenced endocrine therapy utilization but were not associated with PFS. Patients with recurrent disease had shorter PFS (P = .0024) than those presenting with de novo metastasis. The presence of visceral metastasis trended toward shorter PFS (P = .051). Similarly, prior endocrine therapy (P = .003) or chemotherapy (P = .036) was associated with shorter PFS. Body mass index was not associated with PFS or with dose interruption and/or modification. While the number of minorities in this analysis is limited (n = 26), these patients as a group had statistically shorter PFS on treatment (P = .002). Conclusions The real-world progression-free survival with CDK4/6 inhibitors mimics that observed in the clinical trial. A number of clinical and demographic features were associated with PFS on CDK4/6 inhibitor-based therapy. Further studies are ongoing to validate these findings incorporating additional cancer centers.

Few germline genetic variants have been robustly linked with breast cancer outcomes. We conducted trans-ethnic meta genome-wide association study (GWAS) of overall survival (OS) in 3973 breast cancer patients from the Pathways Study, one of the largest prospective breast cancer survivor cohorts. A locus spanning the UACA gene, a key regulator of tumor suppressor Par-4, was associated with OS in patients taking Par-4 dependent chemotherapies, including anthracyclines and anti-HER2 therapy, at a genome-wide significance level ($$P = 1.27 \times 10^{ - 9}$$ P = 1.27 × 1 0 − 9 ). This association was confirmed in meta-analysis across four independent prospective breast cancer cohorts (combined hazard ratio = 1.84, $$P = 1.28 \times 10^{ - 11}$$ P = 1.28 × 1 0 − 11 ). Transcriptome-wide association study revealed higher UACA gene expression was significantly associated with worse OS ($$P = 4.68 \times 10^{ - 7}$$ P = 4.68 × 1 0 − 7 ). Our study identified the UACA locus as a genetic predictor of patient outcome following treatment with anthracyclines and/or anti-HER2 therapy, which may have clinical utility in formulating appropriate treatment strategies for breast cancer patients based on their genetic makeup.

Severe caloric-restriction compromises thyroid hormone (TH) status, apparently to save energy and proteins for enduring stress stimulus. However, a persistent decrease in TH levels may compromise heart function. We hypothesized that supplementation of low dose active TH or targeting hypoxia-inducible factor-1-alpha, HIF-1α (a strong activator of deiodinase enzyme that degrades peripheral active THs) will prevent deterioration of cardiac performance. Adult mice were subjected to acute fasting based on institutional animal protocols with ad libitum access to water. The following groups were studied: Control mice with free access to food; severe caloric restriction fasting only group; Fasting with Triiodo-l-Thyronine (T3); Fasting with HIF-1α inhibitor (BAY). Cardiac hemodynamic and electrophysiological studies were performed and role of long noncoding RNAs were explored. Following severe caloric-restriction, we found that body weights, and heart weights to a partial extent, were decreased. Low-dose T3 treatment attenuated left ventricular hemodynamic impairment in indices of cardiac contractility and relaxation. In electrophysiology studies, fasting mice developed atrial tachyarrhythmias upon induction. This reverted to control levels following T3 treatment. There was a significant increase in atrioventricular conduction time and significant decrease in heart rate following fasting. Both these changes were attenuated following T3 treatment. Furthermore, BAY partially improved hemodynamics. Compared to the severe caloric-restriction group, both T3 and BAY reduced MALAT1 and GAS5 long noncoding RNA expression. These new findings indicate that T3 and BAY protect from cardiac decompensation secondary to acute severe caloric-restriction partly mediated by long noncoding RNAs.

Introduction: The 2017 ACC/AHA guidelines lowered the threshold for blood pressure goals and emphasized incorporation of cardiovascular risk assessment and lifestyle modifications. Due to this update, the prevalence of hypertension increased from 31.9% to 45.6% of Americans. We hypothesized that our patients were not being assessed and counseled in accordance with the 2017 ACC/AHA guidelines at our resident clinic in New York City. Methods: Patients with a diagnosis of hypertension who had at least one office visit between July to September of 2018 at our clinic were included. Patients not seen by a resident physician were excluded. Variables collected included lowest blood pressure reading from visit, comorbidities, and demographics (age, language, race, and gender). The most recent progress note was reviewed for the assessment of hypertension. Additionally, residents of all levels completed an electronic anonymous survey to assess knowledge of updated guidelines. Results: Of the 206 patients meeting inclusion and not exclusion criteria, 148 (71.8%) were above blood pressure goal. The average blood pressure was 137/82 (CI 95%, 134.7-139.3/80.6-83.4). Of those 148 patients not at goal, 108 (72.97%) were incorrectly identified as at goal or did not have hypertension assessed at all. Of the total 206 patients, only 16 (7.77%) had documented discussion of lifestyle modification and 1 patient (0.5%) had an atherosclerotic cardiovascular disease (ASCVD) score in the assessment. Patients with an established resident primary care physician (n=118) were not more likely to meet goal blood pressure (p=0.58) than those who did not. A total of 27 of 78 (34.6%) residents completed the survey, and only 15% (4 of 27) answered all questions correctly. Conclusions: Our hypertensive patients are not meeting their blood pressure goals and often the assessment is insufficient. We are not reliably identifying patients with elevated blood pressure per the 2017 ACC/AHA guidelines and missing opportunities for optimizing care. Enhancing resident understanding of guidelines and evaluation of hypertension is important for meeting blood pressure targets and reducing cardiovascular risk. An intervention to improve resident education and documentation is underway.

Introduction: Stress, anxiety and depression are nontraditional risk factors for cardiovascular disease (CVD) that are more common in women. Yoga and meditation have shown to improve patient’s overall levels of depression, anxiety, and stress, and possibly decrease CVD risk. Hypothesis: We hypothesize that regular, supervised sessions of chair yoga and meditation can be a complementary measure to decrease the level of anxiety, stress and depression in women with or at risk for CVD, and pursue lifestyle modifications. Methods: An anonymous survey was provided to the participants of a weekly complimentary chair yoga/meditation workshop supervised by a trained cardiac yoga therapist. The surveys were distributed on day 1 and on week 24 to assess any changes in their reported level of stress, depression, anxiety and lifestyle. Results: A total of 16 and 10 female participants with or at risk for CVD completed the initial and follow up survey respectively, which included validated screening tools for depression, anxiety and stress. The Patient Health Questionnaire-9 from the initial session to the follow up survey, showed an increase in the score (2.25 vs 3.2 respectively [P = 0.199]). Despite this increased trend, the severity remained within the definition of minimal depression. The mean Generalized Anxiety Disorder-7 went from 7 in the initial visit down to 4.9 (P = 0.138) for the follow up survey (decreased from a definition of mild anxiety to no clinical anxiety). Lastly, the Perceived Stress Score demonstrated a mean reduction from 18.25 to 15.2 (P = 0.106), both remaining as moderate perceived stress. Participants also endorsed a trend towards integrating more low saturated fat foods, and 37.5% endorsed a 3-9 lbs weight loss. Conclusion: Although more research and larger studies are yet to be done to demonstrate a definitive benefit in meditation and gentle chair yoga in CVD risk reduction, our pilot study demonstrated a trend towards overall improvement of novel risk factors for CVD, which predominantly affect women. Given the low harm and cost of these measures, they can be done as adjuvants to our standard of care to increase the patient’s overall well being by improving the psychological aspect of their lives which in turn could reflect on their physical health.

Introduction: Congestive heart failure (CHF) admissions place a financial burden on patients and the healthcare system. The national direct medical costs of CHF have reached $20.9 billion and a CHF related hospitalization costs $14,631 per patient. Studies have demonstrated an association between early post-discharge follow up within 7 days and a reduction in readmission rates. Our study attempts to characterize the rates of follow up appointments in patients discharged from the medicine service in an urban academic hospital. Hypothesis: We hypothesized the rate of early follow-up appointments provided to patients with a diagnosis of an acute CHF exacerbation will be low. Methods: We performed a chart review of patients admitted to our institution from January 2016- February 2017 to the medicine service, including regular medicine floor and telemetry units, with a primary or secondary discharge diagnosis of acute systolic or diastolic heart failure. Discharge paperwork was reviewed for presence of an appointment with a primary care physician (PCP) or cardiologist scheduled within 7 days of discharge, including date and time of appointment. Patients discharged from the cardiology or other services and patients with dispositions of hospice or death were excluded. Results: Over a 13 month period, 63 patients were discharged from the medicine service with a primary or secondary diagnosis of CHF, twelve patients were excluded due to disposition. Among 51 patients, 15.7% (CI 95%, 0.07-0.286) were scheduled for follow-up appointment within 7 days of discharge with a PCP or cardiologist and 2 patients had appointments documented after 7 days. Therefore, 80.4% of patients (CI 95%, 0.695-0.913) did not have any scheduled follow up on their discharge summaries. Conclusion: In conclusion, the majority of CHF patients admitted to the medicine service of our institution are not provided appointments within 7 days of discharge. Data has shown that early follow up appointments are associated with reduced readmission rates. Lowering CHF readmissions are important for reducing medical complications and financial burden on patients and the healthcare system. Our future interventions will focus on increasing the number of patients with appropriate 7 day follow up with the aim to reduce readmissions and medical complications.

Background: The restoration of walking ability in the spinal cord injury (SCI) population is an increasingly important goal in physical therapy. Locomotor training (LT) is often implemented with the aim to restore ambulation. At this point, there are no guidelines for LT in the pediatric SCI population. Objectives: The aim of this review is to further narrow the effects of LT to the pediatric SCI population and develop recommendations for pediatric LT. Methods: A thorough search was performed using the following databases: Scopus, CINAHL, PubMed, and Ovid. Studies were selected based on the following inclusion criteria: pediatric SCI population, articles published within last 10 years, human subjects, and LT. Studies looking at other neurological disorders and subjects who were not previously ambulatory were excluded. Five students and one Faculty Research Advisor from the university's Doctor of Physical Therapy Program evaluated the inclusion criteria, conducted a risk of bias assessment using the Downs and Black checklist, and extracted the results. Results: Six studies were selected for this review. They showed gains in distance, gait speed, walking independence, and participation. There were variations in results when comparing gains in injury level based on the International Standards for Neurological Classification of Spinal Cord Injury (ISNCSCI). Conclusions: Currently there is insufficient evidence to determine the best clinical practice guidelines for rehabilitation using LT within the pediatric SCI population.

Quantification of protein concentrations is often a static and tissue destructive technique. Paired-agent imaging (PAI) using matched targeted and untargeted agents has been established as a dynamic method for quantifying the extracellular domain of epidermal growth factor receptor (EGFR) in vivo in a variety of tumor lines. Here we extend the PAI model to simultaneously quantify the extracellular and intracellular regions of EGFR using novel cell membrane permeable fluorescent small molecules, TRITC-erlotinib (targeted) and BODIPY-N-erlotinib (non-binding control isoform) synthesized in house. An EGFR overexpressing squamous cell carcinoma cell xenograft tumor, A431, was implanted on the chorioallantoic membrane (CAM) of the embryonated chicken egg. In total six fluorescent molecules were administered and monitored over 1 h using multi-spectral imaging. EGFR concentrations were determined using both extracellular and intracellular PAI methods. The fluorescent molecules used for extracellular PAI were ABY-029, an anti- EGFR Affibody molecule conjugated to IRDye 800CW, and a Control Imaging Agent Affibody molecule conjugated to IRDye 680RD. The intracellular PAI (iPAI) fluorescent molecules were cell membrane penetrating TRITC-erlotinib, BODIPY-N-erlotinb, and BODIPY TR carboxylate, as well as cell membrane impermeant control agent, Alexa Fluor 647 carboxylate. Results from simultaneous imaging of both the extracellular and intracellular binding domains of EGFR indicate that concentrations of intracellular EGFR are higher than extracellular. This is anticipated as EGFR exists in two distinct populations in cells, cell membrane bound and internalized, activated protein. iPAI is a promising new method for quantifying intracellular proteins in a rapid tumor model on the chicken CAM.

Tools for rapid therapeutic selection for pancreatic ductal adenocarcinoma (PDAC) patients are vital to improved survival as PDAC is the third leading cause of cancer death, with an average life expectancy of 5-7 months post diagnosis. Treatment options are limited to surgery and chemotherapy, where Gemcitabine has been the cornerstone of therapy since 1997. However, Gemcitabine resistance prevents PDAC cure and mechanisms of resistance are not fully understood. Yet, with average survival times still

Novel mechanisms associated with therapeutically safe thyroid hormone (TH) therapy are emerging. We have shown that oral triiodo-L-thyronine (T3) offers safe cardioprotection in coronary ligation myocardial infarction (MI), ligation ischemia-reperfusion injury, diabetic cardiomyopathy, etc. via restoration of gene expression. However, safe therapeutic effects following atherosclerosis-driven MI and role of long noncoding RNAs (lncRNAs) is unknown. We employed a mouse model of scavenger receptor B1 knockout with hypomorphic apolipoprotein E. Young adult heterozygote littermates served as controls and all mice received high fat (HF) diet for one month. Along with HF diet, a cohort of homozygotes (HypoE) received therapeutic dose of T3 (5.5 μg/kg/d) in drinking water ad libitum. In HypoE mice, Paigen HF diet induced interstitial fibrotic MI with severe hypertrophic (Heart wt./Body wt., HW/BW: control:4.6±0.14; HypoE:12.9±0.75; p2-fold; p

Pancreatic ductal adenocarcinomas (PDAC) are notoriously difficult to treat and in general, molecular targeted therapies have failed even when the targeted protein is overexpressed in the tumor tissue. Genetic mutations in extracellular receptors and downstream signaling proteins (i.e., RAS signaling pathway) and convoluted intracellular cross-talk between cell signaling pathways are likely reasons that these promising therapies fail. Monitoring the complex relationship between intracellular protein signaling is difficult and to-date, standard techniques that are used (Western blot, flow cytometry, immunohistochemistry, etc.) are invasive, static and do not accurately represent in vivo structure-function relationships. Here, we describe the development of an in ovo avatar using patient derived tumors grown on the chicken chorioallantoic membrane (CAM) and the novel fluorescence-based Quantitative Protein Expression Tracking (QUIET) methodology to bridge the gap between oncology, genomics and patient outcomes. Previously developed paired-agent imaging, was extended to a three-compartment model system in QUIET, which utilizes three types of imaging agents: novel fluorophore conjugated cell permeable targeted and untargeted small molecule paired-agents, in addition to a tumor perfusion agent that is not cell membrane permeable. We have demonstrated the ability to quantify the intracellular binding domain of a trans-membrane protein in vitro using cell permeable fluorescent agents (erlotinib-TRITC and control isotype-BODIPY FL). In addition, we have demonstrated imaging protocols to simultaneously image up to 6 spectrally distinct organic fluorophores in in ovo avatars using the Nuance EX (Perkin Elmer) and established proof-of-principle intracellular and extracellular protein concentrations of epidermal growth factor receptor using QUIET and traditional paired-agent imaging.

On two sites in south Mississippi, growth and survival of two oak species, Shumard oak ( Quercus shumardii ) and swamp chestnut oak ( Quercus michauxii ), and three planting stocks: 1-0 bareroot, conventional containerized, and EKOgrown® seedlings, were compared and evaluated for two years. Survival was assessed monthly during the first growing season and at the end of each growing season. Height and groundline diameter were assessed initially after planting and at the end of each growing season. After two growing seasons, Shumard oak exhibited superior performance generally when compared to swamp chestnut oak. EKOgrown® seedlings had poor survival likely caused by negative influences of competing vegetation. Bareroot seedlings performed better than other planting stocks, additionally, the cost efficacy of these seedlings justifies why bareroot planting stocks are superior in most cases of artificial regeneration of hardwoods.

Combining the Capability Approach (CA) with Sustainable Development (SD) is a promising project that has gained much attention. Recently, scholars from both perspectives have worked on narrowing gaps between these development approaches, with a focus on the connection between the CA as a partial justice theory and SD as a concept embracing justice and ecological fragility and relative scarcity. We argue that to base an SD conception on the CA, the CA must be further developed. To provide the rationale for this claim, we begin by clarifying how we look upon the relation between SD and the CA and how we understand SD (1). We then argue for an integration of the natural dimension in the CA (2). By analyzing similarities of recent contributions integrating the natural dimension, we identify how the CA structure may be developed to include the recursive relation between the human and natural dimensions and especially to include the circumstances of justice relevant to SD (3). Finally, we argue that a new recur...

There is a broad differential diagnosis for patients presenting with acute chest pain. History, physical examination, electrocardiogram, and serial troponin assays are pivotal in assessing patients with suspected acute coronary syndrome. However, if the initial workup is equivocal, physicians are faced with a challenge to find the optimal strategy for further triage. Risk stratification scores have been validated for patients with known acute coronary syndrome, such as the TIMI and GRACE scores, but there may be limitations in undifferentiated chest pain patients. Advancements in imaging modalities such as coronary computed tomography angiography and the addition CT derived fractional flow reserve, have demonstrated utility in evaluating patients presenting with acute chest pain. With this article, we aim to provide a comprehensive review of the non-invasive modalities that are available to evaluate acute chest pain patients suspected of cardiac etiology in the emergency room. We also added a focus on new imaging modalities that have shown to have prognostic implications in stable ischemic heart disease.

Background: Stress, anxiety, and depression are nontraditional risk factors for cardiovascular disease (CVD) that are more common in women. For nearly four decades, we have seen a steady decline in the number of deaths in women related to heart disease, especially in those >65 years old. However, recent data suggests there has been a stagnation among women