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Статті в журналах з теми "Research Subject Categories – MEDICINE: cell biology"
Song, Lei, Jiaqi Liang, Wenting Wang, Jie Gao, Hua Chai, Yu Tan, Liying Zheng, Mei Xue, and Dazhuo Shi. "Global Trends in Research of Mitochondrial Biogenesis over past 20 Years: A Bibliometric Analysis." Oxidative Medicine and Cellular Longevity 2023 (January 4, 2023): 1–17. http://dx.doi.org/10.1155/2023/7291284.
Повний текст джерелаSEMUKHINA, ELENA. "ON THE CULTURAL-ETHIC CATEGORIES TRANSFORMATION IN EUROPE OF THE XIX CENTURY: SEARCH FOR THE BASIC FOUNDATIONS." Культурный код, no. 2023-1 (2023): 38–49. http://dx.doi.org/10.36945/2658-3852-2023-1-38-49.
Повний текст джерелаKulkarni, Roshni, Amy D. Shapiro, Jerzy Windyga, Margaret V. Ragni, K. John Pasi, Margareth Castro Ozelo, Elisa Tsao, and Baisong Mei. "Low Bleeding Rates with Increase or Maintenance of Physical Activity in Patients Treated with Recombinant Factor IX Fc Fusion Protein (rFIXFc) in the B-LONG and Kids B-LONG Studies." Blood 126, no. 23 (December 3, 2015): 2307. http://dx.doi.org/10.1182/blood.v126.23.2307.2307.
Повний текст джерелаEckstein, Olive S., Nitya Gulati, Lisa Forbes, Erin Peckham-Gregory, Nmazuo Wudo Ozuah, M. Cecilia Poli, Tiphanie Vogel, et al. "Genomic Characterization of a Pediatric Cohort with Non-Malignant Lymphoproliferative Disorders." Blood 134, Supplement_1 (November 13, 2019): 83. http://dx.doi.org/10.1182/blood-2019-131884.
Повний текст джерелаMuzyka, Logan, Nicolas K. Goff, Nikita Choudhary, and Michael T. Koltz. "Systematic Review of Molecular Targeted Therapies for Adult-Type Diffuse Glioma: An Analysis of Clinical and Laboratory Studies." International Journal of Molecular Sciences 24, no. 13 (June 21, 2023): 10456. http://dx.doi.org/10.3390/ijms241310456.
Повний текст джерелаTalalaeva, Galina. "Dynamics of Representations Concerning Mechanisms of Formation of Social Identity of Youth: a Review of Publications of the RSCI." DEMIS. Demographic Research 2, no. 3 (October 7, 2022): 89–103. http://dx.doi.org/10.19181/demis.2022.2.3.7.
Повний текст джерелаZhou, Yifan, Minwen Zhou, Min Gao, Haiyun Liu, and Xiaodong Sun. "Factors Affecting the Foveal Avascular Zone Area in Healthy Eyes among Young Chinese Adults." BioMed Research International 2020 (March 24, 2020): 1–8. http://dx.doi.org/10.1155/2020/7361492.
Повний текст джерелаFink-Puches, Regina, Paulus Zenahlik, Barbara Bäck, Josef Smolle, Helmut Kerl, and Lorenzo Cerroni. "Primary cutaneous lymphomas: applicability of current classification schemes (European Organization for Research and Treatment of Cancer, World Health Organization) based on clinicopathologic features observed in a large group of patients." Blood 99, no. 3 (February 1, 2002): 800–805. http://dx.doi.org/10.1182/blood.v99.3.800.
Повний текст джерелаFarooq, Muhammad, Aman Ullah Khan, Hosny El-Adawy, Katja Mertens-Scholz, Iahtasham Khan, Heinrich Neubauer, and Yuh-Shan Ho. "Research Trends and Hotspots of Q Fever Research: A Bibliometric Analysis 1990-2019." BioMed Research International 2022 (January 15, 2022): 1–14. http://dx.doi.org/10.1155/2022/9324471.
Повний текст джерелаBoyle, Molly H., Bindu Bennet, Karyn Colman, Anna-Lena Frisk, Begonya Garcia, Christopher D. Houle, Annette Romeike, Radhakrishna Sura, Jonathan Werner, and Susan A. Elmore. "Publication Categories in Toxicologic Pathology." Toxicologic Pathology 49, no. 5 (February 12, 2021): 1042–47. http://dx.doi.org/10.1177/0192623321992305.
Повний текст джерелаДисертації з теми "Research Subject Categories – MEDICINE: cell biology"
Di, Franco Giovanna. "Valutazione della risposta, su colture cellulari di melanoma, della radiozione fotonica e protonica nell'associzione radiochemioterapica." Thesis, Università degli Studi di Catania, 2011. http://hdl.handle.net/10761/248.
Повний текст джерелаOrobello, Sara. "Studio dei meccanismi patogenetici attraverso l'analisi di tessuti periferici e linee cellulari nella malattia di Huntington per la ricerca di nuovi biomarkers." Thesis, Universita' degli Studi di Catania, 2011. http://hdl.handle.net/10761/101.
Повний текст джерелаHuntington disease (HD) is the most common and well-studied polyglutamine neurodegenerative disorder. It has a prevalence of 3- 10 affected subjects per 100000 individuals in Western Countries (Rawlins 2010; Spinney 2010). The disorder was first clinically described as a familial neuropsychiatric disease in the 19th century by George Huntington, but the responsible gene and its mutation were identified in 1993 (Huntington's Disease Collaborative Research Group 1993). Since then, the knowledge on clinical and molecular aspects of the disease has been increasing exponentially. HD is an autosomal dominant neurodegenerative disorder caused by the expansion of an unstable CAG triplet repeat beyond 36 in the HTT gene (Kremer et al. 1994), which codes for a large and ubiquitously expressed protein named huntingtin (htt). The mutation length influences the age at onset and the disease progression, the expansion homozygosity causing a particularly more severe disease course and neuropathology (Squitieri et al., 2003). Although, most of cases show an age at onset around 40s, the disease may start early in the life or very late in the elderly according to the penetrance of the mutation (Rubinsztein et al., 1996). This leaves the pathology unpredictable in at risk individuals who undergo a predictive genetic test and discovery to be mutation carriers, the number of CAG repeats accounting for only 60-70% of the age at onset variation. Other factors of biological and/or environmental origin including gene modifiers contribute therefore to the beginning and development of the disease (Squitieri et al., 2000a; Wexler et al., 2004). Only when the mutation is particularly expanded and toxic, the disease starts in children even very early in life with a devastating course (Quarrel et al. 2009). Therefore the age at onset unpredictability of most HD cases and the progression variability among patients strongly advises to search for markers sensitive enough to monitor the devolopmet of the pathological process in absence of symptoms in unaffected at risk subjects. Similarly, markers to test the progression of the disease other than the symptom changes would be crucial for monitoring the efficacy of further, yet unavailable, therapies, in symptomatic patients. Good biomarkers should be easy to get from mutation carrier subjects and must reflect a pathogenic mechanism of the disease. So far, no validate markers have been described and introduced into the clinical practice.
Giudice, Aurelio. "Basi di conoscenza e tecniche di Data Mining con applicazioni agli RNA non codificanti." Thesis, Università degli Studi di Catania, 2011. http://hdl.handle.net/10761/187.
Повний текст джерелаGarcía, Pedro Emilio. "Importancia pronóstica del marcador Ki67 en los tumores de glándulas salivales: estudio clínico patológico." Doctoral thesis, García PE. Importancia pronóstica del marcador Ki67 en los tumores de glándulas salivales: estudio clínico patológico [Internet]. [Córdoba]: Universidad Nacional de Córdoba; 2019 [citado el 13 de febrero de 2020]. Disponible en: https://rdu.unc.edu.ar/handle/11086/14018, 2019. http://hdl.handle.net/11086/14018.
Повний текст джерелаFil: Garcia, Pedro Emilio. Universidad Nacional de Córdoba. Facultad de Ciencias Médicas. Cátedra Biología Celular, Histología y Embriología; Argentina.
Introducción: Los tumores de glándulas salivales son un grupo poco frecuente y heterogéneo de neoplasias, lo que implica dificultades tanto en el diagnóstico como en el pronóstico de esta patologia. Ki67 es un marcador que se expresa en las células en división, se ha visto que está asociado a mayor agresividad en distintos tipos de tumores, y se ha observado en varios estudios que un valor elevado está relacionado con una peor evolución de los pacientes con neoplasias de glándulas salivales. El objetivo de este trabajo fue demostrar la importancia de Ki67 como factor pronóstico en los pacientes con tumores de glándulas salivales tratados con radioterapia. Material y Métodos: Se evaluaron los pacientes con tumores de glándulas salivales localizados, tratados con radioterapia en el Instituto Zunino; se realizó marcación de Ki67 por inmunohistoquimica; se lo estratificó en alto (mayor de 20%), bajo (entre 1% y 20%) y negativo (menor o igual a 1%); y se relacionó la expresión con el porcentaje de recidivas, metástasis a distancia y muertes por enfermedad. Se realizó el cálculo de sobrevida global, sobrevida libre de recidiva, sobrevida libre de metástasis y sobrevida causa específica. Resultados: Se estudiaron 48 pacientes tratados entre 2005 y 2015. Vientiún pacientes(43,7%) tenían Ki67 alto, 21 (43,7%) Ki67 bajo; y 6 (12,6%), Ki67 negativo. El seguimiento medio fue de 48,5 meses. 15 (31,25%) pacientes fallecieron; 11 en el grupo de Ki67 alto, 2 en el grupo de Ki67 bajo y 2 pacientes en el grupo en que fue negativo. Todas las muertes por cáncer fueron por metástasis a distancia; solo 2 pacientes presentaron recidiva locorregional, la cual fue tratada con cirugía o nuevo esquema de radioterapia. La sobrevida global para todo el grupo fue de 85% a 12 meses y 79% a 24 meses. La sobrevida global a 2 años para el grupo de Ki67 alto fue de 67%, mientras que para el grupo de Ki67 bajo y negativo fue de 96%, lo cual es estadísticamente significativo(p<0.015). La sobrevida libre de metástasis a 2 años fue 57% para los pacientes con Ki67 alto, mientras que para los Ki67 bajo-negativo, esta fue de 85%. Estas diferencias fueron significativas (p<0,0008); mientras que no hubo diferencias en la sobrevida libre de recidiva local. Conclusiones: Una alta expresión de Ki67 está asociado con mayor número de metástasis y muertes por enfermedad, con peor sobrevida en los pacientes con tumores de glándulas salivales.
Introduction: Salivary gland tumors are a rare and heterogeneous group of neoplasms, which implies difficulties both in the diagnosis and in the prognosis of this disease. Ki67 is a marker that is expressed in dividing cells, it has been found to be associated with greater aggressiveness in different types of tumors, and it has been observed in several studies that a high value is related to a worse evolution of patients with Salivary gland neoplasms. The objective of this work was to demonstrate the importance of Ki67 as a prognostic factor in patients with salivary gland tumors treated with radiotherapy. Material and Methods: Patients with localized salivary gland tumors treated with radiotherapy at the Zunino Institute were evaluated; Ki67 labeling was performed by immunohistochemistry; it was stratified in high (greater than 20%), low (between 1% and 20%) and negative (less than or equal to 1%); and the expression was related to the percentage of relapses, distant metastases and deaths due to disease. The calculation of global survival, free survival of recurrence, survival free of metastasis and survival specific cause was made. Results: 48 patients treated between 2005 and 2015 were studied. Twenty-one patients (43.7%) had high Ki67, 21 (43.7%) Ki67 low; and 6 (12.6%), Ki67 negative. The mean follow-up was 48.5 months. 15 (31.25%) patients died; 11 in the high Ki67 group, 2 in the low Ki67 group and 2 patients in the negative group. All deaths from cancer were due to distant metastases; Only 2 patients had locoregional recurrence, which was treated with surgery or a new radiotherapy regimen. Overall survival for the entire group was 85% at 12 months and 79% at 24 months. The 2-year global survival for the Ki67 high group was 67%, while for the Ki67 low and negative group it was 96%, which is statistically significant (p <0.015). Metastasis free survival at 2 years was 57% for patients with high Ki67, while for Ki67 low-negative, this was 85%. These differences were significant (p <0.0008); while there were no differences in the free survival of local recurrence. Conclusions: A high expression of Ki67 is associated with a greater number of metastasis and deaths due to disease, with worse survival in patients with salivary gland tumors.
2021-10-07
Maniscalchi, Eugenia Tiziana. "Alterazione secretoria nel diabete mellito: ruolo dell'alfa cellula pancreatica." Thesis, Universita' degli Studi di Catania, 2011. http://hdl.handle.net/10761/351.
Повний текст джерелаThis study investigated in a pancreatic alfa-cell line the effects of chronic exposure to palmitate on the insulin and IGF-I receptor (IGF-IR) and intracellular insulin pathways. alfa-TC1â 6 cells were cultured in the presence or absence of palmitate (0.5 mmol/liter) up to 48 h. Glucagon secretion, insulin and IGF-IR autophosphorylation, and insulin receptor substrate (IRS)-1, IRS-2, phosphatidylinositol kinase (PI3K) (p85alfa), and serine-threonine protein kinase (Akt) phosphorylated (active) forms were measured. Erk 44/42 and p38 phosphorylation (P) (MAPK pathway markers) were also measured. Because MAPK can regulate Pax6, a transcription factor that controls glucagon expression, pairedboxgene6 (Pax6) and glucagon gene and protein expression were also measured. Basal glucagon secretion was increased and the inhibitory effect of acute insulin exposure reduced in alfa-TC1 cells cultured with palmitate. Insulin-stimulated insulin receptor phosphorylation was greatly reduced by exposure to palmitate. Similar results were observed with IRS-1-P, PI3K (p85 alfa), and Akt-P. In contrast, with IGF-IR and IRS-2-P, the basal levels (i.e. in the absence of insulin stimulation) were higher in cells cultured with palmitate. Similar data were obtained with Erk 44/42-P and p-38-P. Pax6 and glucagon gene and protein expression were higher in cells cultured with palmitate. In these cells cultured, specifics MAPKs inhibitors were able to reduce both Pax6 and glucagon gene and protein expression. These results indicate that alfa-cells exposed to palmitate show insulin resistance of the IRS-1/PI3K/Akt pathway that likely controls glucagon secretion. In contrast, the IRS-2/MAPKs pathway is stimulated, through an activation of the IGF-IR, leading to increased Pax6 and glucagon expression. Our data support the hypothesis that the chronic elevation of fatty acids contribute to alfa-cell dysregulation frequently observed in type 2 diabetes.
Malaguarnera, Roberta. "Carcinoma tiroideo: vie di trasduzione del segnale coinvolte nella tumorigenesi tiroidea ed efficacia di terapie molecolare multiple." Thesis, Universita' degli Studi di Catania, 2011. http://hdl.handle.net/10761/350.
Повний текст джерелаIntroduction: In thyroid follicular cells, TSH, acting through cAMP, regulates cell growth and requires mTOR to exert its mitogenic response. In poorly differentiated thyroid carcinomas and in human thyroid cancer cell lines the TSH dependence for growth is lost, although mTOR pathway is still activated. MAPK and PI3K pathways are central in thyroid cancer pathogenesis and may converge to mTOR cascade. Thus, these cascades could be responsible for mTOR activation and thyroid cell proliferation. Material and Methods: we employed non-transformed thyroid rat cells (PPCL3) and human thyroid cancer cell lines harboring mutations in thyroid oncoproteins RET/PTC, RAS and BRAF. Aims: 1) to evaluate whether TSH/cAMP/PKA signaling pathway regulates mTOR activation and its proliferative response; 2) to study the role of the thyroid oncoproteins RET/PTC3, HRASG12V or BRAFV600E in regulating mTOR activity in our in vitro models; 3) to investigate the efficacy of combined targeting of MAPK, PI3K and mTOR signaling cascades in inhibiting growth and proliferation of human thyroid cancer cell lines. Results: 1) in PCCL3 cells, TSH/cAMP/PKA cascade was central in mediating mTOR signals. In contrast, thyroid cancer cell lines switched the control of mTOR activation from the TSH/cAMP/PKA signals to either MAPK and/or PI3K; 2) conditional expression of the oncoproteins RET/PTC3, HRASG12V and BRAFV600E induced mTOR activity in PPCL3 cells. Moreover, mTOR was required for DNA synthesis induced by all three oncoproteins; 3) rapamycin alone suppressed growth of human thyroid cancer cell lines to a variable degree, whereas the combination of mTOR, MEK and AKT1/2 inhibitors significantly suppressed growth in all cell lines analyzed, except for those addicted mainly to only one survival pathway. Conclusions: In thyroid cancer cells in which multiple parallel cascades (i.e. mTOR, MAPK and PI3K) mediate the survival signals, the multi-targeted therapy could be exploited to achieve optimal therapeutic benefits.
Majorana, Alessandra. "Alterazioni specifiche del trascrittoma dei microrna e struttura globale del network in carcinoma colorettale dopo trattamento con Cetuximab." Thesis, American Association for Cancer Research, 2011. http://hdl.handle.net/10761/129.
Повний текст джерелаThe relationship between therapeutic response and modifications of miRNA transcriptome in Colorectal Cancer (CRC) remains unknown. We investigated this issue by profiling the expression of 667 miRNAs in two human CRC cell lines, one sensitive and the other resistant to cetuximab(Caco-2 and HCT-116, respectively) through TaqMan RT-PCR. Caco-2 and HCT-116 expressed different sets of miRNAs after treatment: specifically, 21 and 22 miRNAs were differentially expressed (DE) in Caco-2 or HCT-116, respectively (t-test, p<0.01). By testing the expression of DE miRNAs in CRC patients, we found that miR-146b-3p and miR-486-5p are more abundant in KRAS mutated samples respect to wild-type ones (Wilcoxon test, p<0.05). 67% of DE miRNAs were involved in cancer, including CRC, while 19 miRNA targets had been previously reported to be involved in the cetuximab pathway and CRC. We identified 25 TFs putatively controlling these miRNAs, 11 of which already reported to be involved in CRC. Based on these data, we suggest that the down regulation of let-7b and let-7e (targeting KRAS) and the up regulation of miR-17* (a CRC marker) could be considered as candidate molecular markers of cetuximab resistance. Global network functional analysis, based on miRNA targets, showed a significant overrepresentation of cancer-related biological processes and networks centered on critical nodes involved in EGFR internalization and ubiquitin-mediated degradation. The identification of miRNAs, whose expression is linked to the efficacy of therapy, should allow to predict the response of patients to treatment and possibly lead to a better understanding of the molecular mechanisms of drug response.