Publications by authors named "Scarpelli D"

Importance: Medication nonadherence leads to worse health outcomes, increased healthcare service utilization, and increased overall healthcare costs.

Objective: To determine whether a discharge pharmacy located in the Emergency Department (ED) reduces ED revisits and hospitalizations.

Design: This is a cohort study where we extracted data from our electronic medical records with adult encounters between 12/2019-10/2021.

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Purpose: Discharge prescriptions represent an important aspect of care for patients seen in the emergency department (ED) setting and are used by providers to continue therapy for acute illness once patients leave the ED or to prevent future exacerbations of chronic conditions. The success of an ED discharge and the medications prescribed rely on patient compliance. Compliance depends on patients' ability to obtain prescriptions, which can be hindered by limited access to pharmacies and cost.

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Article Synopsis
  • A case study of a 6-year-old girl presented severe symptoms from a high-grade AVM, leading to surgery and initial SRS treatment, but she later developed recurrent symptoms due to a new AVM nidus.
  • The treatment for her persistent RIN shifted from steroids to bevacizumab, resulting in a significant improvement in her symptoms and reduced side effects associated with long-term steroid use.
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  • The study analyzed demographics, treatment methods, and outcomes for meningeal melanocytomas using data from the National Cancer Database for cases from 2002 to 2016.
  • The results showed a median survival of about 57 months and a 5-year overall survival rate of 48%, with higher income correlating with better survival outcomes.
  • Although surgery was the primary treatment, radiotherapy was given to 37.7% of patients but did not improve survival; limitations in treatment data affected further analysis.
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Single-fraction stereotactic radiosurgery (SRS) is a highly used tool in managing brain metastases, alongside its multifraction counterpart - stereotactic body radiation therapy (SBRT). These radiation therapy techniques have been associated with excellent clinical outcomes, such as decreased local recurrence, increased survival, and improved palliative effects. However, present literature concerning the cost-effectiveness of these techniques remain scarce.

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Background: Pleomorphic xanthoastrocytomas (PXAs) account for <1% of primary brain tumors, occurring predominantly in children and young adults. Surgical resection serves as the primary treatment for PXAs, while radiotherapy (RT) and chemotherapy protocols remain poorly defined.

Aim: This study aims to determine current care patterns utilized for pediatric patients (≤ 18 years) diagnosed with PXAs and their effect on overall survival.

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Myxopapillary ependymomas (MPE) are WHO Grade I ependymomas that annually occur in 0.05-0.08 per 100,000 people.

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Background: Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of endothelial nitric oxide synthase, which was associated with insulin resistance. Dimethylarginine dimethylaminohydrolase (DDAH) is the major determinant of plasma ADMA. Examining data from the DIAGRAM+ (Diabetes Genetics Replication And Meta-analysis), we identified a variant (rs9267551) in the DDAH2 gene nominally associated with type 2 diabetes (P = 3 × 10(-5)).

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Context: The prevalence of type 2 diabetes (T2D), particularly among young adults, has been rising steadily during the past 2 decades. T2D, especially in its early-onset subtype, is under genetic control. TRIB3 inhibits insulin-stimulated Akt phosphorylation and subsequent insulin action.

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Interleukin (IL)-10 is a major anti-inflammatory cytokine that has been associated with obesity and type 2 diabetes. The three polymorphisms -1082G/A, -819C/T, and -592C/A in the IL10 promoter were reported to influence IL10 transcription. We investigated whether these polymorphisms were associated with type 2 diabetes and related traits in a cohort of Italian Caucasians comprising 551 type 2 diabetic and 1,131 control subjects.

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Context: RET mutation analysis provides useful information on the clinical outcome of medullary thyroid carcinomas (MTCs) and the risk of disease in the family members.

Objective: The objective of this study was to document genotype-phenotype relationships in an Italian family with a novel RET mutation.

Design/setting: RET gene alterations were investigated in a patient with unifocal MTC and her relatives.

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Background: Recovery of iodide uptake in thyroid cancer cells by means of obtaining the functional expression of the sodium/iodide symporter (NIS) represents an innovative strategy for the treatment of poorly differentiated thyroid cancer. However, the NIS gene expression alone is not always sufficient to restore radioiodine concentration ability in these tumour cells.

Methods: In this study, the anaplastic thyroid carcinoma ARO cells were stably transfected with a Pax8 gene expression vector.

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Primary hyperparathyroidism (pHPT) is a common endocrine disease that in more than 95% of cases is sporadic and only in some cases is caused by inherited disorders, isolated or as part of multiple endocrine neoplasia (MEN1 and 2). Somatic mutations of MEN1 gene have also been described in sporadic parathyroid tumors. In our study, we examined the presence of alterations in MEN1 gene in a series of 39 patients who had undergone surgery for sporadic pHPT (35 with parathyroid adenoma or hyperplasia, 4 with a carcinoma).

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Sodium/iodide symporter (NIS) expression has recently been described in human breast cancer, with emphasis on its potential exploitation for the treatment of these tumors with radioiodine. In this study, we analyzed the regulation of NIS expression and function in the MCF-7 human breast cancer cell line. Cell exposure to insulin, IGF-I, IGF-II, or prolactin induced significant increases in 125I uptake and the expression of both NIS mRNA and NIS protein.

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Causative gain-of-function mutations of the RET tyrosine-kinase receptor gene have been reported in more than 95% of inherited cases of medullary thyroid carcinoma (MTC; OMIM# 155240). Most RET activating mutations are clustered in mutational "hot spots" in exons 10, 11, 13, 14, 15 and 16 and are usually detected by single-strand conformation polymorphism (SSCP) followed by direct sequencing. To improve sensitivity, time and costs of mutational screening we have developed a denaturing high performance chromatography (DHPLC) protocol, based on the detection of heteroduplex molecules by ion-pair reverse-phase liquid chromatography under partially denaturing conditions.

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Ten years after the first description of activating mutations in the thyroid stimulating hormone receptor (TSHR) gene in sporadic autonomous hyperfunctioning thyroid adenomas, there is general agreement in assigning a major pathogenic role of this genetic abnormality, acting via the constitutive activation of the cAMP pathway, in both the growth and functional characteristic of these tumours. From the beginning, however, the pathophysiological and clinical relevance of somatic TSHR mutations has been debated and some arguments still exist against a fully causative role of these mutations and the practical value of detecting these mutations for the diagnosis, treatment and prognosis of thyroid hot nodules. Some major issues will be examined herein, including (a) the frequency of TSHR alterations in various reports showing that the genetic abnormality underlying the pathogenesis of a substantial subset of thyroid tumours has yet to be identified; (b) the limitations of the present experimental models, which suggest greater caution in the interpretation of in vitro results; (c) the still unresolved question of absence of genotype-phenotype correlation.

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Hyperfunctioning thyroid nodules are characterized by the presence of spontaneous somatic mutations responsible for constitutive activation of the cAMP pathway. However, alterations affecting other elements of the cAMP signaling system may counteract the effects of the mutations. In this study, the expression of the adenylyl cyclase (AC) types III and VI was investigated by Western blot in 18 hyperfunctioning thyroid nodules; in 12 samples, we also assessed the presence of TSH receptor (TSHR) or gsp mutations and levels of AC VI and III mRNA.

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Background: Various clinical and experimental findings support the concept that human chorionic gonadotropin (hCG) can stimulate iodide uptake in thyroid cells.

Design: We investigated the molecular mechanisms underlying the effects of hCG on iodide uptake, and particularly its action on the expression of Na+/I- symporter (NIS) mRNA and protein.

Methods: Iodide uptake was analyzed in FTRL-5 cells by measuring (125)I concentrations in cells after a 30-min exposure to 0.

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Sodium/iodide symporter (NIS) gene and protein expressions have been recently described in human cytotrophoblasts, emphasizing its potential function in the active transport of iodide from the mother to the fetus. In this study we analyzed NIS expression and function in the human JAr placental choriocarcinoma cell line. Using real-time quantitative RT-PCR, we first demonstrated that NIS transcripts are expressed at a high level in JAr cells compared with other cell lines, including thyroid cancer cells.

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Objective: In the present study we analyzed the pattern of pendrin (PDS) and sodium/iodide symporter (NIS) gene expression in some thyroid carcinoma cell lines and a series of thyroid tumoral tissues.

Methods: Total RNA was extracted from all cell lines and from 53 tissues, and gene expression was examined by RT-PCR. Semiquantitative 'multiplex' RT-PCR was used to assess variations in PDS gene expression among various thyroid pathologies.

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One of the tight junction components, zonula occludens protein 2 (ZO-2), is expressed as two isoforms, ZO-2A and ZO-2C, in normal epithelia. In pancreatic adenocarcinoma of the ductal type ZO-2A is absent, but none of the common mechanisms of gene inactivation is responsible for lack of ZO-2A expression. In the current study, we report the complete organization of the human zo-2 gene (tjp-2), its alternative splicing, and its expression in normal and neoplastic tissues of several organ sites.

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