Publications by authors named "Andreea Pop"

Objectives: This study focuses on the factors that encouraged engagement in research activities, as well as the barriers that restricted their involvement, until the final year of study at Iuliu Hatieganu University of Medicine and Pharmacy Cluj-Napoca, Faculty of Medicine. The main objectives of this study are to investigate potential disparities in research culture and student engagement in various research opportunities between Romanian and international medical graduates, as well as to conduct an examination of the observed patterns across various graduating years (2021-2023).

Materials And Methods: A cross-sectional investigation was conducted among graduate students of the Faculty of Medicine at the Iuliu Hațieganu University of Medicine and Pharmacy in Cluj-Napoca, Romania.

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Introduction: This study focuses on the influence of the COVID-19 pandemic on medical students in their last year of study at the Faculty of Medicine of the University of Medicine and Pharmacy in Cluj-Napoca, Romania. It analyzes the impact of social distance limits on the conduct of research activities required for the development of the graduation thesis, as well as assesses sixth-year students' attitudes and behaviors toward volunteer activities during the COVID-19 pandemic.

Methods: A cross-sectional survey was conducted in June-July 2021 among sixth-year students.

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Objectives: This study focuses on the assessment of attitudes and practices regarding research among undergraduate medical students from Cluj-Napoca, Romania.

Material And Methods: A cross-sectional study was performed thorough anonymous questionnaires (May-June 2018) among 510 third- and fifth-year students of Iuliu Hatieganu University of Medicine and Pharmacy from Cluj-Napoca, Romania.

Results: More than 60% of the third- and fifth-year students declared that they were interested and willing to perform research during medical studies, while more than two-thirds were interested in doing so after graduation.

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Cognitive impairment and learning ability of the brain are directly linked to synaptic plasticity as measured in changes of long-term potentiation (LTP) and long-term depression (LTD) in animal models of brain diseases. LTD reflects a sustained reduction of the synaptic AMPA receptor content based on targeted clathrin-mediated endocytosis. AMPA receptor endocytosis is initiated by dephosphorylation of Tyr on the C-terminus of the AMPAR subunit GluA2.

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The orthodontic miniscrew (TADs) is a device that is fixed into bone in the short term for the purpose of enhancing orthodontic anchorage. The aim of our study was to investigate the structural and surface properties of recovered TADs after orthodontic treatment, and compare them to new TADs. TADs (n = 15) from the same manufacturer (Absoanchor; Dentos, Daegu, Korea) were assessed; n = 10 were recovered from patients after orthodontic treatment and n = 5 were new.

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Patients with anticoagulant therapy have a high thromboembolic risk. Due to the rich oro-maxillofacial vasculature and the fact that some dental procedures may cause a bleeding, the physician should be able to correlate this risk with the hemorrhagic risk. Dental procedures are a trigger for psychic stress.

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Introduction: Fragile X syndrome (FXS) is a common monogenetic cause of intellectual disability, autism spectrum features, and a broad range of other psychiatric and medical problems. FXS is caused by the lack of the fragile X mental retardation protein (FMRP), a translational regulator of specific mRNAs at the postsynaptic compartment. The absence of FMRP leads to aberrant synaptic plasticity, which is believed to be caused by an imbalance in excitatory and inhibitory network functioning of the synapse.

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Background And Aims: Obesity proved to favor clinical decompensation in patients with cirrhosis. Our aim was to investigate if metabolic syndrome (MS) in cirrhotic patients represents a risk factor for decompensation.

Methods: 704 cirrhotics, included in a MS prevalence study were considered for evaluation; 121 patients were excluded because they did not complete the follow-up and 303 because they were decompensated at the start of the study.

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Rationale: Fragile X syndrome (FXS) is considered the leading inherited cause of intellectual disability and autism. In FXS, the fragile X mental retardation 1 (FMR1) gene is silenced and the fragile X mental retardation protein (FMRP) is not expressed, resulting in the characteristic features of the syndrome. Despite recent advances in understanding the pathophysiology of FXS, there is still no cure for this condition; current treatment is symptomatic.

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Cerebellar granule cells (GCs) account for more than half of all neurons in the CNS of vertebrates. Theoretical work has suggested that the abundance of GCs is advantageous for sparse coding during memory formation. Here, we minimized the output of the majority of GCs by selectively eliminating their CaV2.

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Fragile X syndrome (FXS) is the leading monogenic cause of intellectual disability and autism. The disease is a result of lack of expression of the fragile X mental retardation protein. Brain tissues of patients with FXS and mice with FMRP deficiency have shown an abnormal dendritic spine phenotype.

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Fragile X syndrome is caused by lack of FMR1 protein (FMRP) leading to severe symptoms, including intellectual disability, hyperactivity and autistic-like behaviour. FMRP is an RNA binding protein involved in the regulation of translation of specific target mRNAs upon stimulation of metabotropic glutamate receptor 5 (mGluR5) at the synapse. The absence of FMRP leads to enhanced activity of mGluR5 signal transduction pathways.

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Fragile X syndrome (FXS) is the most common inherited form of mental retardation and is caused by the lack of fragile X mental retardation protein (FMRP). In the brain, spine abnormalities have been reported in both patients with FXS and Fmr1 knockout mice. This altered spine morphology has been linked to disturbed synaptic transmission related to altered signaling in the excitatory metabotropic glutamate receptor 5 (mGluR5) pathway.

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Fragile X syndrome, the most common form of inherited intellectual disability, is caused by a lack of FMRP, which is the product of the Fmr1 gene. FMRP is an RNA-binding protein and a component of RNA-granules found in the dendrites of neurons. At the synapse, FMRP is involved in regulation of translation of specific target mRNAs upon stimulation of mGluR5 receptors.

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