Weakness After an Intra-articular Steroid Injection: A Case Report of Acute Steroid-induced Myopathy.

INTRODUCTION: Weakness is a common chief complaint in the emergency department, and the use of glucocorticoids is pervasive in medicine. Muscle weakness, or myopathy, is a well documented side effect of chronic glucocorticoid use. However, acute myopathy, with an onset shortly after initiation of glucocorticoids, is much rarer. CASE REPORT: We present a case of acute steroid-induced myopathy after a single intra-articular dose of triamcinolone in a young, healthy, active male. To our knowledge, this is the first case described in the medical literature of acute steroid-induced myopathy following a single intra-articular injection. CONCLUSION: In a patient who presents with proximal muscle weakness and has a history of glucocorticoid use, the diagnosis of steroid-induced myopathy should be considered. Acute steroid-induced myopathy should be high on the differential in a patient who presents with typical symptoms and has been prescribed glucocorticoids for less than 14 days or, in rare cases, may have recently received a single dose of glucocorticoids. Treatment is supportive and outpatient management is typically indicated, as respiratory muscle involvement is rare.

Supporting Undergraduate Biology Students' Academic Success: Comparing Two Workshop Interventions.

College students' performance in introductory-level biology course work is an important predictor of ongoing persistence in the major. This study reports on a researcher-educator partnership that designed and compared two cocurricular workshops. Seventeen laboratory sections of an undergraduate biology course were randomly assigned to one of two educational interventions during the regularly scheduled lab class section after students had completed and received the results for the first exam. The baseline Metacognition intervention was an hourlong workshop focused on effective learning strategies and self-awareness in the learning process; the extended Metacognition plus Time Management (Metacognition+TM) intervention included the aforementioned workshop plus a second hourlong workshop on time management and procrastination. Based on three exams and self-report surveys administered before the intervention and at the end of the semester, students who participated in the Metacognition+TM intervention experienced greater increases in their exam scores and degree commitment than those in the baseline intervention. Additionally, group status moderated the effect of the intervention, as the Metacognition+TM intervention was especially effective in increasing use of time management tools by students from minoritized groups.

Growth of Crystalline Bimetallic Metal-Organic Framework Films via Transmetalation.

Crystalline films of the Cu3(BTC)2 (BTC3- = 1,3,5-benzenetricarboxylate) metal-organic framework (MOF) have been grown by dip-coating an alumina/Si(111) substrate in solutions of Cu(II) acetate and the organic linker H3BTC. Atomic force microscopy (AFM) experiments demonstrate that the substrate is completely covered by the MOF film, while grazing incidence wide-angle X-ray scattering (GIWAXS) establishes the crystallinity of the films. Forty cycles of dip-coating results in a film that is ∼70 nm thick with a root mean squared roughness of 25 nm and crystallites ranging from 50-160 nm in height. Co2+ ions were exchanged into the MOF framework by immersing the Cu3(BTC)2 films in solutions of CoCl2. By varying the temperature and exchange times, different concentrations of Co were incorporated into the films, as determined by X-ray photoelectron spectroscopy experiments. AFM studies showed that morphologies of the bimetallic films were largely unchanged after transmetalation, and GIWAXS indicated that the bimetallic films retained their crystallinity.

Opioid Addiction in Pregnancy: Does Depression Negatively Impact Adherence With Prenatal Care?

OBJECTIVE: We aimed to evaluate whether depression in pregnancy in women with opioid dependency negatively impacts adherence with prenatal care. METHODS: This was a retrospective chart analysis of opioid-dependent pregnant women over a 6-year period at 2 large referral and tertiary care centers. The primary outcome was adherence with prenatal care based on the concurrent diagnosis of depression. Adherence was assessed by looking at the number of observed versus expected prenatal visits. Secondary outcomes included neonatal intensive care unit (NICU) stay, and incidence and severity of neonatal abstinence syndrome (NAS). RESULTS: A total of 74 patient charts were reviewed. 45/74 (60.8%) of the opioid-dependent pregnant patients were either diagnosed with depression (n = 41), anxiety (n = 2), or scored >10 on the Edinburgh Prenatal Depression Scale (n = 1). Patients with a diagnosis of depression were significantly less adherent with prenatal care; 80% adherent (73% vs 93%; P = 0.03), 90% adherent (62% vs 93%; P = 0.003). A higher number of patients in the depression group had an infant treated for withdrawal (62% vs 38%; P = 0.041), and had longer NICU stays (27% vs 21%; P = 0.018). Analysis of the whole cohort of opioid dependent gravidas revealed Buprenorphine maintenance therapy had the lowest mean NAS score 6.5 ±â€Š4.4, compared with methadone maintenance 10.6 ±â€Š3.6, and no maintenance therapy 9.4 ±â€Š4.0 (P = 0.008). CONCLUSION: Depression negatively impacts adherence with prenatal care and was significantly associated with a higher incidence of neonatal withdrawal and longer NICU stays. Buprenorphine therapy had the lowest incidence and severity of NAS when compared with methadone and no maintenance therapy.

Improving Pre-Service Teachers' Performance Skills Through Behavioral Skills Training.

In higher education, instruction that incorporates effective performance skills training is vital to equipping pre-service teachers with the tools they will use to educate children. This study evaluated the effects of behavioral skills training (BST) on performance of evidence-based practices by undergraduate pre-service special education teachers. A pre-post design was used to evaluate performance during role-play. BST sessions produced higher levels of correct performance than baseline measures across all seven participants. We discuss limitations of these results with suggestions for future research, along with recommendations for incorporating BST into university settings.

Radiation therapy may increase metastatic potential in alveolar rhabdomyosarcoma.

BACKGROUND: We previously determined that radiation could be safely administered using a mouse-flank in vivo model to both alveolar (Rh30) and embryonal (Rh18) rhabdomyosarcoma xenografts. Mice from both tumor lines in this experiment developed metastases, an event not previously described with these models. We sought to determine if radiation-induced changes in gene expression underlie an increase in the metastatic behavior of these tumor models. PROCEDURE: Parental Rh18 and Rh30 xenografts, as well as tumor that recurred locally after radiotherapy (Rh18RT and Rh30RT), were grown subcutaneously in the flanks of SCID mice and then subjected to either fractionated radiotherapy or survival surgery alone. Metastasis formation was monitored and recorded. Gene expression profiling was also performed on RNA extracted from parental, recurrent, and metastatic tissue of both tumor lines. RESULTS: Rh30 and Rh30RT xenografts demonstrated metastases only if they were exposed to fractionated radiotherapy, whereas Rh18 and Rh18RT xenografts experienced significantly fewer metastatic events when treated with fractionated radiotherapy compared to survival surgery alone. Mean time to metastasis formation was 40 days in the recurrent tumors and 73 days in the parental xenografts. Gene expression profiling noted clustering of Rh30 recurrent and metastatic tissue that was independent of the parental Rh30 tissue. Rh18RT xenografts lost radiosensitivity compared to parental Rh18. CONCLUSION: Radiation therapy can significantly decrease the formation of metastases in radio-sensitive tumors (Rh18) and may induce a more pro-metastatic phenotype in radio-resistant lines (Rh30).

FANCD2 is a potential therapeutic target and biomarker in alveolar rhabdomyosarcoma harboring the PAX3-FOXO1 fusion gene.

PURPOSE: Alveolar rhabdomyosarcoma that harbors the PAX3-FOXO1 fusion gene (t-ARMS) is a common and lethal subtype of this childhood malignancy. Improvement in clinical outcomes in this disease is predicated upon the identification of novel therapeutic targets. EXPERIMENTAL DESIGN: Robust mouse models were used for in vivo analysis, and molecular studies were performed on xenografts treated in parallel. Two independent patient sets (n = 101 and 124) of clinically annotated tumor specimens were used for analysis of FANCD2 levels and its association with clinical and molecular characteristics and outcomes. RESULTS: Our xenograft studies reveal a selective suppression of FANCD2 by m-TOR kinase inhibition and radiosensitization of the t-ARMS line only. In the initial patient set, we show that FANCD2 transcript levels are prognostic in univariate analysis, and are significantly associated with metastatic disease and that the copresence of the translocation and high expression of FANCD2 is independently prognostic. We also demonstrate a significant and nonrandom enrichment of mTOR-associated genes that correlate with FANCD2 gene expression within the t-ARMS samples, but not within other cases. In the second patient set, we show that on a protein level, FANCD2 expression correlates with PAX3-FOXO1 fusion gene and is strongly associated with phospho-P70S6K expression in cases with the fusion gene. CONCLUSIONS: Our data demonstrate that FANCD2 may have a significant role in the radiation resistance and virulence of t-ARMS. Indirectly targeting this DNA repair protein, through mTOR inhibition, may represent a novel and selective treatment strategy.

PTSD symptoms and somatic complaints following Hurricane Katrina: the roles of trait anxiety and anxiety sensitivity.

This study examined the relationships between trait anxiety and anxiety sensitivity and the outcome variables posttraumatic stress disorder (PTSD) symptoms and somatic complaints following a major hurricane. Sixth and seventh graders in the New Orleans area (N = 302) were surveyed 5 to 8 months following Hurricane Katrina. As expected, hurricane exposure was a significant predictor of PTSD symptoms and somatic symptoms. Also as hypothesized, certain factors of anxiety sensitivity interacted with trait anxiety to predict PTSD symptoms and somatic symptoms. Clinical implications of potential linkages among trait anxiety, dimensions of anxiety sensitivity and PTSD, and somatic symptoms are discussed.

TNF is a key mediator of septic encephalopathy acting through its receptor, TNF receptor-1.

In this study, we demonstrate that mice deficient in TNFR1 (TNFR1(-/-)) were resistant to LPS-induced encephalopathy. Systemic administration of lipopolysaccharide (LPS) induces a widespread inflammatory response similar to that observed in sepsis. Following LPS administration TNFR1(-/-) mice had less caspase-dependent apoptosis in brain cells and fewer neutrophils infiltrating the brain (p<0.039), compared to control C57Bl6 (TNFR1(+/+)) mice. TNFR1-dependent increase in aquaporin (AQP)-4 mRNA and protein expression was observed with a concomitant increase in water content, in brain (18% increase in C57Bl6 mice treated with LPS versus those treated with saline), similar to cerebral edema observed in sepsis. Furthermore, absence of TNFR1 partially but significantly reduced the activation of astrocytes, as shown by immunofluorescence and markedly inhibited iNOS mRNA expression (p<0.01). Septic encephalopathy is a devastating complication of sepsis. Although, considerable work has been done to identify the mechanism causing the pathological alterations in this setting, the culprit still remains an enigma. Our results demonstrate for the first time that endotoxemia leads to inflammation in brain, with alteration in blood-brain barrier, up-regulation of AQP4 and associated edema, neutrophil infiltration, astrocytosis, as well as apoptotic cellular death, all of which appear to be mediated by TNF-alpha signaling through TNFR1.

The role of the complement cascade in endotoxin-induced septic encephalopathy.

The complement system normally eliminates bacteria and has a protective effect. However, in an inflammatory setting such as sepsis, an exaggerated or insufficient activation of this cascade can have deleterious effect through the activation of glial cells, secretion of proinflammatory cytokines and generation of other toxic products. The aim of the present study was to investigate the role of the complement cascade in septic encephalopathy, through the passive injection of endotoxin/lipopolysaccharide (LPS) into mice overexpressing the potent complement inhibitor, CR1-related y (Crry-tg). Increased gliosis occurred in brains of endotoxemic mice. Concomitant with this, there was a significant rise in mRNA expression of GFAP, CD45 and proinflammatory molecules, TLR4, TNF-alpha and NO, in these brains. Consistent with the capacity of these inflammatory mediators, there was increased apoptosis as determined by DNA fragmentation and TUNEL staining on LPS treatment, which occurred through the Akt pathway. In addition, there was increased water content in brain, similar to cerebral edema observed in sepsis. Relative to wild-type mice, complement-inhibited mice had an attenuated inflammatory response, decreased edema and reduced apoptosis. Therefore, we demonstrate for the first time that the complement cascade appears to be one of the key players that cause brain pathology in an endotoxemic setting and therefore is a viable therapeutic target.