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Introduction: Acquired MET gene amplification, MET exon 14 skip mutations, or MET fusions can emerge as resistance mechanisms to tyrosine kinase inhibitors (TKIs) in patients with lung cancer. The efficacy and safety of combining MET TKIs (such as crizotinib, capmatinib, or tepotinib) with parent TKIs to target acquired MET resistance are not well characterized. Methods: Multi-institutional retrospective chart review identified 83 patients with metastatic oncogene-driven NSCLC that were separated into the following two pairwise matched cohorts: (1) MET cohort (n = 41)—patients with acquired MET resistance continuing their parent TKI with a MET TKI added or (2) Chemotherapy cohort (n = 42)—patients without any actionable resistance continuing their parent TKI with a platinum-pemetrexed added. Clinicopathologic features, radiographic response (by means of Response Evaluation Criteria in Solid Tumors version 1.1), survival outcomes, adverse events (AEs) (by means of Common Terminology Criteria for Adverse Events version 5.0), and genomic data were collected. Survival outcomes were assessed using Kaplan-Meier methods. Multivariate modeling adjusted for lines of therapy, brain metastases, TP53 mutations, and oligometastatic disease. Results: Within the MET cohort, median age was 56 years (range: 36–83 y). Most patients were never smokers (28 of 41, 68.3%). Baseline brain metastases were common (21 of 41, 51%). The most common oncogenes in the MET cohort were EGFR (30 of 41, 73.2%), ALK (seven of 41, 17.1%), and ROS1 (two of 41, 4.9%). Co-occurring TP53 mutations (32 of 41, 78%) were frequent. Acquired MET alterations included MET gene amplification (37 of 41, 90%), MET exon 14 mutations (two of 41, 5%), and MET gene fusions (two of 41, 5%). After multivariate adjustment, the objective response rate (ORR) was higher in the MET cohort versus the chemotherapy cohort (ORR: 69.2% versus 20%, p

PURPOSEThe purpose of this mixed-methods psychometric study was to translate and adapt the Arabic Pain Care Quality (APainCQ) Survey to Arabic and to measure the quality of pain care provided to Arab patients.PATIENTS AND METHODSThis study used an iterative, mixed-methods approach that employed cognitive interviews, expert content analysis, and factor analysis to develop the APainCQ Survey. The study was conducted at Dubai Hospital, Dubai Health Authority, United Arab Emirates. Arabic-speaking patients admitted to the oncology/hematology inpatient units with a minimum 24-hour stay were eligible for the study.RESULTSThe sample consisted of 155 patients. The iterative exploratory factor analysis process resulted in the sequential removal of three items. The results of the significant Bartlett test (P < .001) of sphericity and Kaiser-Meyer-Olkin test of 0.93 for both the health care team scale and the nurse scale. The total variance explained was 76.17% for the health care team scale and 60.91% for the nurse scale, which explained 56.51% for factor 1 with 14 items and 4.40% for factor 2. Regarding internal consistency reliability, Cronbach's alpha and McDonald's omega for the health care team scale and nurse scale were high; both values were .95. Internal consistency reliability of pain assessment and pain management subscales of nurse scales were also high, with values of 0.96 and 0.79, respectively. Moreover, there was a moderate correlation (r = 0.66; P < .001) between the two subscales in the nurse scale.CONCLUSIONThis study provides evidence that the APainCQ is a reliable and valid measure of pain dimensions, including pain management and monitoring. This APainCQ scale can potentially expand research and clinical assessment in the Arab world.

Sex estimation of skeletons is fundamental to many archaeological studies. Currently, three approaches are available to estimate sex-osteology, genomics, or proteomics, but little is known about the relative reliability of these methods in applied settings. We present matching osteological, shotgun-genomic, and proteomic data to estimate the sex of 55 individuals, each with an independent radiocarbon date between 2,440 and 100 cal BP, from two ancestral Ohlone sites in Central California. Sex estimation was possible in 100% of this burial sample using proteomics, in 91% using genomics, and in 51% using osteology. Agreement between the methods was high, however conflicts did occur. Genomic sex estimates were 100% consistent with proteomic and osteological estimates when DNA reads were above 100,000 total sequences. However, more than half the samples had DNA read numbers below this threshold, producing high rates of conflict with osteological and proteomic data where nine out of twenty conditional DNA sex estimates conflicted with proteomics. While the DNA signal decreased by an order of magnitude in the older burial samples, there was no decrease in proteomic signal. We conclude that proteomics provides an important complement to osteological and shotgun-genomic sex estimation.

Abstract Patients with metastatic NSCLC bearing a ROS1 gene fusion usually experience prolonged disease control with ROS1-targeting tyrosine kinase inhibitors (TKI), but significant clinical heterogeneity exists in part due to the presence of co-occurring genomic alterations. Here, we report on a patient with metastatic NSCLC with a concurrent ROS1 fusion and KRAS p.G12C mutation at diagnosis who experienced a short duration of disease control on entrectinib, a ROS1 TKI. At progression, the patient continued entrectinib and started sotorasib, a small molecule inhibitor of KRAS p.G12C. A patient-derived cell line generated at progression on entrectinib demonstrated improved TKI responsiveness when treated with entrectinib and sotorasib. Cell-line growth dependence on both ROS1 and KRAS p.G12C was further reflected in the distinct downstream signaling pathways activated by each driver. Clinical benefit was not observed with combined therapy of entrectinib and sotorasib possibly related to an evolving KRAS p.G12C amplification identified on repeated molecular testing. This case supports the need for broad molecular profiling in patients with metastatic NSCLC for potential therapeutic and prognostic information.

The use of hybrid photovoltaic/thermal (PV/T) and low concentrating photovoltaic/thermal (LCPV/T) systems can significantly enhance the overall solar energy conversion efficiency by delivering electricity and thermal energy. This paper presents a case study using a standing PV system's theoretical and modeling approach that can be modified to adapt to the hybrid technology. Firstly, a single-pass conventional PV/T air-cooled collector is investigated based on heat transfer and electrical models under the climatic conditions of Zarqa, Jordan. The performance parameters are evaluated using thermal and electrical properties of the considered PV installation and measured meteorological data. Results show that the total energy produced varies between a maximum of 134.6 kWh/m2 in July and a minimum of 81.7 kWh/m2 in January. The annual average hourly variation of overall energy efficiency ranges between 79.2% and 88.4%. Moreover, the dissipated thermal energy can meet 63.6% of the total energy required to ventilate the Hashemite University Presidency Building during the winter months. Finally, the performance of the modeled PV/T system air system coupled with flat boosters to provide a low irradiation concentration ratio (CR) is explored. The maximum electric output of the resulting LCPV/T system is compared with the uncooled system. It is found that the percentage improvement due to air cooling ranges between 0.72% at CR=1 and 2.77% at CR=2.5

Abstract Background ROS1 tyrosine kinase inhibitors (TKIs) have demonstrated significant clinical benefit for ROS1+ NSCLC patients. However, TKI resistance inevitably develops through ROS1 kinase domain (KD) modification or another kinase driving bypass signaling. While multiple TKIs have been designed to target ROS1 KD mutations, less is known about bypass signaling in TKI‐resistant ROS1+ lung cancers. Methods Utilizing a primary, patient‐derived TPM3‐ROS1 cell line (CUTO28), we derived an entrectinib‐resistant line (CUTO28‐ER). We evaluated proliferation and signaling responses to TKIs, and utilized RNA sequencing, whole exome sequencing, and fluorescence in situ hybridization to detect transcriptional, mutational, and copy number alterations, respectively. We substantiated in vitro findings using a CD74‐ROS1 NSCLC patient's tumor samples. Last, we analyzed circulating tumor DNA (ctDNA) from ROS1+ NSCLC patients in the STARTRK‐2 entrectinib trial to determine the prevalence of MET amplification. Results CUTO28‐ER cells did not exhibit ROS1 KD mutations. MET TKIs inhibited proliferation and downstream signaling and MET transcription was elevated in CUTO28‐ER cells. CUTO28‐ER cells displayed extrachromosomal (ecDNA) MET amplification without MET activating mutations, exon 14 skipping, or fusions. The CD74‐ROS1 patient samples illustrated MET amplification while receiving ROS1 TKI. Finally, two of 105 (1.9%) entrectinib‐resistant ROS1+ NSCLC STARTRK‐2 patients with ctDNA analysis at enrollment and disease progression displayed MET amplification. Conclusions Treatment with ROS1‐selective inhibitors may lead to MET‐mediated resistance. The discovery of ecDNA MET amplification is noteworthy, as ecDNA is associated with more aggressive cancers. Following progression on ROS1‐selective inhibitors, MET gene testing and treatments targeting MET should be explored to overcome MET‐driven resistance.

Abstract EGFR mutant non-small cell lung cancer patients' disease demonstrates remarkable responses to EGFR-targeted therapy, but inevitably they succumb to acquired resistance, which can be complex and difficult to treat. Analyzing acquired resistance through broad molecular testing is crucial to understanding the resistance mechanisms and developing new treatment options. We performed diverse clinical testing on a patient with successive stages of acquired resistance, first to an EGFR inhibitor with MET gene amplification and then subsequently to a combination EGFR and MET targeted therapies. A patient-derived cell line obtained at the time of disease progression was used to identify NRAS gene amplification as an additional driver of drug resistance to combination EGFR/MET therapies. Analysis of downstream signaling revealed extracellular signal-related kinase activation that could only be eliminated by trametinib treatment, while Akt activation could be modulated by various combinations of MET, EGFR, and PI3K inhibitors. The combination of an EGFR inhibitor with a MEK inhibitor was identified as a possible treatment option to overcome drug resistance related to NRAS gene amplification.

Summary: Lipid phosphate phosphatases are a family of enzymes with diverse cellular metabolic functions. Phospholipid phosphatase 6 (PLPP6) is a regulator of cellular polyisoprenyl phosphates; however, its in vivo functions remain to be determined. Here, mouse PLPP6 was characterized to possess similar catalytic properties as the human enzyme. Plpp6 knockout mice (Plpp6−/−) were generated and displayed decreased airway allergen sensitization, pointing to a role for PLPP6 in the early events of lung allergic responses. Dendritic cell (DC) responses were investigated and endocytosis of allergen via macropinocytosis was decreased in Plpp6−/− DCs that had lower cholesterol content. When reversed by cholesterol loading, the DC macropinocytosis defect is corrected. Adoptive transfer of Plpp6−/− DCs to wild-type mice during sensitization was sufficient to decrease allergen-induced responses. Together, our findings have identified PLPP6 as a pivotal regulator of DC cholesterol content and macropinocytosis, cellular mechanisms that are important for pathologic responses in allergen-induced lung inflammation.

IntroductionVirtual patient care has seen incredible growth since the beginning of the COVID-19 pandemic. To provide greater access to safe and timely urgent care, in the fall of 2020, the Ministry of Health introduced a pilot program of 14 virtual urgent care (VUC) initiatives across the province of Ontario. The objective of this paper was to describe the overall design, facilitators, barriers, and lessons learned during the implementation of seven emergency department (ED) led VUC pilot programs in Ontario, Canada.MethodsWe assembled an expert panel of 13 emergency medicine physicians and researchers with experience leading and implementing local VUC programs. Each VUC program lead was asked to describe their local pilot program, share common facilitators and barriers to adoption of VUC services, and summarize lessons learned for future VUC design and development.ResultsModels of care interventions varied across VUC pilot programs related to triage, staffing, technology, and physician remuneration. Common facilitators included local champions to guide program delivery, provincial funding support, and multi-modal marketing and promotions. Common barriers included behaviour change strategies to support adoption of a new service, access to high-quality information technology to support new workflow models that consider privacy, risk, and legal perspectives, and standardized data collection which underpin overall objective impact assessments.ConclusionsThese pilot programs were rapidly implemented to support safe access to care and ED diversion of patients with low acuity issues during the COVID-19 pandemic. The heterogeneity of program implementation respects local autonomy yet may present challenges for sustainability efforts and future funding considerations.

ABSTRACT Influenza A virus (IAV) infections are a leading cause of mortality worldwide. Excess mortality during IAV epidemics and pandemics is attributable to secondary bacterial infections, particularly pneumonia caused by Streptococcus pneumoniae. Resident alveolar macrophages (rAMs) are early responders to respiratory infections that coordinate initial host defense responses. Maresin conjugates in tissue regeneration (MCTRs) are recently elucidated cysteinyl maresins that are produced by and act on macrophages. Roles for MCTRs in responses to respiratory infections remain to be determined. Here, IAV infection led to transient decreases in rAM numbers. Repopulated lung macrophages displayed transcriptional alterations 21 days post-IAV with prolonged susceptibility to secondary pneumococcal infection. Administration of a mix of MCTR1 to 3 or MCTR3 alone post-IAV decreased lung inflammation and bacterial load 48 and 72 h after secondary pneumococcal infection. MCTR-exposed rAMs had increased migration and phagocytosis of Streptococcus pneumoniae, reduced secretion of CXCL1, and a reversion toward baseline levels of several IAV-induced pneumonia susceptibility genes. Together, MCTRs counter regulated post-IAV changes in rAMs to promote a rapid return of bacteria host defense. IMPORTANCE Secondary bacterial pneumonia is a serious and common complication of IAV infection, leading to excess morbidity and mortality. New host-directed approaches are needed to complement antibiotics to better address this important global infectious disease. Here, we show that harnessing endogenous resolution mechanisms for inflammation by exogenous administration of a family of specialized proresolving mediators (i.e., cys-MCTRs) increased macrophage resilience mechanisms after IAV to protect against secondary infection from Streptococcus pneumoniae.

Aim: The SAMe-TT2R2 score helps identify patients with atrial fibrillation (AF) likely to have poor anticoagulation control during anticoagulation with vitamin K antagonists (VKA) and those with scores >2 might be better managed with a target-specific oral anticoagulant (NOAC). We hypothesized that in clinical practice, VKAs may be prescribed less frequently to patients with AF and SAMe-TT2R2 scores >2 than to patients with lower scores. Methods and results: We analyzed the Phase III dataset of the Global Registry on Long-Term Oral Antithrombotic Treatment in Patients with Atrial Fibrillation (GLORIA-AF), a large, global, prospective global registry of patients with newly diagnosed AF and ≥1 stroke risk factor. We compared baseline clinical characteristics and antithrombotic prescriptions to determine the probability of the VKA prescription among anticoagulated patients with the baseline SAMe-TT2R2 score >2 and ≤ 2. Among 17,465 anticoagulated patients with AF, 4,828 (27.6%) patients were prescribed VKA and 12,637 (72.4%) patients an NOAC: 11,884 (68.0%) patients had SAMe-TT2R2 scores 0-2 and 5,581 (32.0%) patients had scores >2. The proportion of patients prescribed VKA was 28.0% among patients with SAMe-TT2R2 scores >2 and 27.5% in those with scores ≤2. Conclusions: The lack of a clear association between the SAMe-TT2R2 score and anticoagulant selection may be attributed to the relative efficacy and safety profiles between NOACs and VKAs as well as to the absence of trial evidence that an SAMe-TT2R2-guided strategy for the selection of the type of anticoagulation in NVAF patients has an impact on clinical outcomes of efficacy and safety. The latter hypothesis is currently being tested in a randomized controlled trial. Clinical trial registration: URL: https://www.clinicaltrials.gov//Unique identifier: NCT01937377, NCT01468701, and NCT01671007.

The distal ulna has always been considered to be expendable and its removal has been advocated for a variety of post-traumatic degenerative and oncological conditions but recent studies showed that the distal radioulnar joint allows supination and protonation of the forearm and is important to one’s grip strength and lifting ability. Several prosthesis models have already been made to replace the mechanical functionality of the distal radioulnar joint. We present two cases of females aged 22 and 12 years, respectively, who presented with wrist pain and swelling without any history of trauma and with terminal degree limitation in wrist movements due to tenderness and swelling. Both of them did not have any distant metastasis upon radiographic staging. The skeletally mature patient underwent radical excision of the distal ulnar osteosarcoma and received a distal radioulnar joint replacement prosthesis (Scheker prosthesis). The other skeletally immature patient underwent radical excision of the involved distal ulnar osteosarcoma with stabilization of the residual ulnar stump using the extensor carpi ulnaris sling in a modified version of the Goldner and Hayes technique. Both of our patients were treated according to the protocols of our multidisciplinary clinic sarcoma team by starting with neoadjuvant chemotherapy, followed by surgery and adjuvant chemotherapy. Both registered an almost complete restoration of the normal wrist and hand function and were in complete remission for 26 and 24 months, respectively. Based on our literature review, these are some of the extremely rare cases in which the osteosarcoma affected an unusual site (the distal ulna where they underwent a rare type of reconstruction status following radical excision of a malignant tumor).

Sepsis is a critical illness characterized by dysregulated inflammatory responses lacking counter-regulation. Specialized proresolving mediators are agonists for antiinflammation and for promoting resolution, and they are protective in preclinical sepsis models. Here, in human sepsis, we mapped resolution circuits for the specialized proresolving mediators resolvin D1 and resolvin D2 in peripheral blood neutrophils and monocytes, their regulation of leukocyte activation and function ex vivo, and their relationships to measures of clinical severity. Neutrophils and monocytes were isolated from healthy subjects and patients with sepsis by inertial microfluidics and resolvin D1 and resolvin D2 receptor expression determined by flow cytometry. The impact of these resolvins on leukocyte activation was determined by isodielectric separation and leukocyte function by stimulated phagolysosome formation. Leukocyte proresolving receptor expression was significantly higher in sepsis. In nanomolar concentrations, resolvin D1 and resolvin D2 partially reversed sepsis-induced changes in leukocyte activation and function. Principal component analyses of leukocyte resolvin receptor expression and responses differentiated sepsis from health and were associated with measures of sepsis severity. These findings indicate that resolvin D1 and resolvin D2 signaling for antiinflammation and resolution are uncoupled from leukocyte activation in early sepsis and suggest that indicators of diminished resolution signaling correlate with clinical disease severity.

Abstract Tuberous Sclerosis Complex (TSC), a rare genetic disorder with mechanistic target of rapamycin complex 1 (mTORC1) hyperactivation, is characterized by multi-organ hamartomatous benign tumors including brain, skin, kidney, and lung (Lymphangioleiomyomatosis). mTORC1 hyperactivation drives metabolic reprogramming including glucose and glutamine utilization, protein, nucleic acid and lipid synthesis. To investigate the mechanisms of exogenous nutrients uptake in Tsc2-deficient cells, we measured dextran uptake, a polysaccharide internalized via macropinocytosis. Tsc2-deficient cells showed a striking increase in dextran uptake (3-fold, p

Purinergic G-protein-coupled receptors are ancient and the most abundant group of G-protein-coupled receptors (GPCRs). The wide distribution of purinergic receptors in the cardiovascular system, together with the expression of multiple receptor subtypes in endothelial cells (ECs) and other vascular cells demonstrates the physiological importance of the purinergic signaling system in the regulation of the cardiovascular system. This review discusses the contribution of purinergic P2Y receptors to endothelial dysfunction (ED) in numerous cardiovascular diseases (CVDs). Endothelial dysfunction can be defined as a shift from a “calm” or non-activated state, characterized by low permeability, anti-thrombotic, and anti-inflammatory properties, to a “activated” state, characterized by vasoconstriction and increased permeability, pro-thrombotic, and pro-inflammatory properties. This state of ED is observed in many diseases, including atherosclerosis, diabetes, hypertension, metabolic syndrome, sepsis, and pulmonary hypertension. Herein, we review the recent advances in P2Y receptor physiology and emphasize some of their unique signaling features in pulmonary endothelial cells.

Angiogenic vasa vasorum (VV) expansion plays an essential role in the pathogenesis of hypoxia-induced pulmonary hypertension (PH), a cardiovascular disease. We previously showed that extracellular ATP released under hypoxic conditions is an autocrine/paracrine, the angiogenic factor for pulmonary artery (PA) VV endothelial cells (VVECs), acting via P2Y purinergic receptors (P2YR) and the Phosphoinositide 3-kinase (PI3K)-Akt-Mammalian Target of Rapamycin (mTOR) signaling. To further elucidate the molecular mechanisms of ATP-mediated VV angiogenesis, we determined the profile of ATP-inducible transcription factors (TFs) in VVECs using a TranSignal protein/DNA array. C-Jun, c-Myc, and Foxo3 were found to be upregulated in most VVEC populations and formed nodes connecting several signaling networks. siRNA-mediated knockdown (KD) of these TFs revealed their critical role in ATP-induced VVEC angiogenic responses and the regulation of downstream targets involved in tissue remodeling, cell cycle control, expression of endothelial markers, cell adhesion, and junction proteins. Our results showed that c-Jun was required for the expression of ATP-stimulated angiogenic genes, c-Myc was repressive to anti-angiogenic genes, and Foxo3a predominantly controlled the expression of anti-apoptotic and junctional proteins. The findings from our study suggest that pharmacological targeting of the components of P2YR-PI3K-Akt-mTOR axis and specific TFs reduced ATP-mediated VVEC angiogenic response and may have a potential translational significance in attenuating pathological vascular remodeling.

The aim of this literature review is to investigate the safest and most appropriate actions for the management of chemotherapy-induced febrile neutropenia. A literature search was undertaken, including major computerized electronic databases (PUBMED, SPRINGER, and WILEY). All studies that discuss colony stimulating factor plus antibiotics versus antibiotics or colony stimulating factors alone for the treatment of febrile neutropenia in adult oncology patients were sought. A review of the selected studies was performed. Most studies focus on the prompt assessment and management for oncology patients who are experiencing febrile neutropenia by using appropriate antibiotics and highlight the importance of using antibiotics and colony stimulating factor in the management of chemotherapy-induced neutropenic fever.Key words: febrile neutropenia, chemotherapy, management, oncology patients

L’objectif de cette recension de la documentation scientifique est de faire enquête sur les méthodes les plus sécuritaires et appropriées de gestion de la neutropénie fébrile induite par la chimiothérapie. Nous avons mené notre recherche documentaire dans les grandes bases de données électroniques (PUBMED, SPRINGER et WILEY). Nous cherchions des études qui discutent de l’alternative entre les thérapies combinant des facteurs de croissance hématopoïétique et des antibiotiques, d’une part, et les thérapies basées sur les antibiotiques ou les facteurs de croissance hématopoïétique seuls, d’autre part, pour le traitement de la neutropénie fébrile parmi les patients adultes en oncologie. La plupart des études retenues étaient axées sur l’évaluation de patients en oncologie atteints d’une neutropénie fébrile et sur la gestion efficace de leur cas au moyen d’antibiotiques appropriés, et elles soulignaient l’importance de l’utilisation d’antibiotiques et de facteurs de croissance hématopoïétique dans la gestion de la fièvre neutropénique induite par la chimiothérapie. Mots clés : neutropénie fébrile, chimiothérapie, gestion, patients en oncologie

Background: Cancer diagnosis has a significant impact not only on women, but also on their Primary caregivers. Understanding the effects of a breast cancer diagnosis on physical and mental health outcomes in caregivers is important because these variables are key components of quality of life. Quality of life is a multi-dimensionalconstruct measuring overall enjoyment of life. This study intends to describe the impact of caring for women with breast cancer on the quality of life among their primary caregivers.Method: We conducted a comprehensive search in PubMed, MEDLINE andCINAHL. In addition, we used the web search engine “Google” for abstracts from 2007 to 2012. A total of eight studies were reviewed that met the following inclusion criteria: adult women with breast cancer, research conducted in English. Studies ranged from 2007-2011. The total sample size in the eight studies on adult caregivers totaled 789 participants. The average age of participants in all of the studies was 49.55 years.There were seven studies that had a quantitative focus,which mainly used a questionnaire and survey to estimate quality of life among primary caregivers. The qualitative approach included in-depth interviews and a focus group.Results: Accumulating evidence has supported the concept that cancer affects not only the patients but also their primary caregiver's quality of life.They face multiple challenges in caring for women with breast cancer, including physical, emotional, social, and financial stress that affects the caregiver's quality of life.Conclusion: Breast cancer diagnosis not only affects the patient's quality of life, but in parallel, also affects the quality of life of the primary caregiver. Thus more focus should be placed on providing moral and social support, and educational resources to improve the level of the caretaker's quality of life.

Effective cancer pain management mandates precise attitude, assessment, skills, and knowledge. Health professionals' knowledge and attitudes concerning cancer pain management have often been referred to as insufficient. This study explored pain knowledge and attitudes of nurses working in oncology settings. Population 115 oncology nurses working at 2 hospitals in the United Arab Emirates. A descriptive, correlational, cross-sectional design was used to examine nurse knowledge and attitudes about pain using the Nurses' Attitude and Knowledge Survey Regarding Pain (NKASRP) survey. NKASRP score differences were examined among nurses with varying demographics, levels of pain education and experience. The mean KASRP was 45%, significantly below the passing score of 80%. Pain management education was not found to have a significant impact on KASRP thus suggesting the need for more effective educational approaches to developing appropriate knowledge and attitudes towards pain among the nurses. No significant differences between sex, educational level, nursing and oncology experience, and nationality or religion were found. The study highlights the need for new initiatives targeting nurses working with cancer patients who are likely to experience significant pain. An ongoing need exists for more effective evidence-based educational programs in cancer pain management. Interactive teaching strategies such as on the job training, improvisational learning, and case studies should be tested for their influence on pain knowledge and attitudes and patient outcomes. [ABSTRACT FROM AUTHOR]

Purpose To evaluate the attitudinal barriers to cancer pain management among adult Jordanian patients and to explore relationships between attitudinal barriers, pain, and demographic variables. Methods In this descriptive correlational study a convenience sample of 150 Jordanian adults with cancer pain were recruited from the outpatient cancer clinic at a regional comprehensive cancer center in Jordan. Patients completed the Arabic version of Barriers Questionnaire (ABQ-II), the Arabic version of Brief-Pain-Inventory (ABPI), and demographic questions. Results More than half of participants were male (61%), had a mean age of 44 years and length of education 14.5 years. Mean (SD) ABQ-II total score was 2.3 (0.8), on a scale of 0–5, with higher scores indicating stronger barriers. Older patients had significantly more barriers, and scored higher on concerns about harmful effects and communication. Patients with higher education levels had significantly lower fatalistic beliefs. Patients with higher barriers had significantly higher levels of worst pain. Pain interference with life activities was positively correlated with the fatalism subscale. Conclusions Study provides useful baseline data on barriers to management of cancer pain among Jordanian that have not been available before. This data can be used in planning and testing interventions to understand and improve patient's attitudes to cancer pain management, and allow for cross-cultural comparisons. [ABSTRACT FROM AUTHOR]

Background & Aims Chronic intake of proton pump inhibitors (PPI) has been associated with hypomagnesemia, but prevalence of PPI-associated hypomagnesemia is not known. Methods We examined the prevalence of hypomagnesemia among long-term PPI recipients by using a large health maintenance organization database. We collected data on 10,167 participants eligible for chronic drug prescriptions from 2008 through 2013. Adult subjects receiving continuous PPI therapy for ≥6 months between 2008 and 2013 and ≥1 serum magnesium determination(s) were identified. Patients with any magnesium levels less than 1.6 mg/dL were selected for analysis; those with recognizable causes of altered magnesium homeostasis were excluded. Results Five hundred ninety participants received long-term PPIs, and 414 (70.2%) met the inclusion criteria for a total exposure of 2293 PPI-years (average, 5.7 years/subject). Of these patients, 57 (13.8%) had ≥1 low serum magnesium; 5 were no longer on PPIs, and 44 had other recognizable causes for hypomagnesemia (25 receiving diuretics, 8 with chronic diarrhea, 8 with chronic kidney disease, and 3 with malignancies). Of the 8 remaining patients (7 female; mean age, 71.2 ± 13.4 years; mean daily medications, 5.4 ± 1.1), mild hypomagnesemia (range, 1.2–1.5 mg/dL) was noted in 13.9% of 289 measurements. All 8 patients had normal serum levels of magnesium at their final measurement. Conclusions In the absence of known precipitating factors, chronic PPI use does not appear to be associated with hypomagnesemia. [ABSTRACT FROM AUTHOR]