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1.
Eur. j. anat ; 21(2): 113-118, abr. 2017. ilus
Artigo em Inglês | IBECS | ID: ibc-163136

RESUMO

Nicotine forms the major addictive component of the tobacco smoke. The pancreas is one of the organs where the metabolic processes of tobacco take place. This work was designed to study the effect of nicotine administration and the effect of its withdrawal on the pancreas of albino rat. Twenty-five male albino rats were separated into two groups. Group I acted as control. Rats in group II received 1.5 mg/kg body weight of nicotine by subcutaneous injection day after day divided into two subgroups, each one containing ten rats. The first one received treatment for 4 months, and then the rats were sacrificed, while the second group received treatment for 4 months, and the rats were sacrificed after one month from treatment stoppage. The pancreases were removed and processed for histological examination and electron microscopy. Histopathological and electron microscopic examination of the pancreas of nicotinetreated rats showed degenerated and distorted pancreatic acini and β cells. These changes included pyknotic nucleus, cytoplasmic swelling, vacuolization and interstitial edema in pancreatic acinar cells. Some of the islets of Langerhans showed vaculation inside their cell and others did not show apparent changes. There was also a significant decrease in lipase and glucose levels. However, after withdrawal of nicotine, the pancreas showed more degenerated pancreatic acini and β cells. There was significant increase in blood glucose level and significant decrease in lipase of treated rats. Nicotine treatment for four months induced histopathological changes in both exocrine and endocrine pancreatic tissue that resemble the picture of chronic pancreatitis. These changes persisted long after cessation of nicotine exposure


No disponible


Assuntos
Animais , Ratos , Pâncreas , Nicotina/efeitos adversos , Tabagismo/diagnóstico , Pancreatite Crônica/induzido quimicamente , Fumar/efeitos adversos , Pâncreas Exócrino , Ilhotas Pancreáticas , Células Secretoras de Insulina , Células Acinares/patologia
2.
Cir. Esp. (Ed. impr.) ; 94(9): 511-517, nov. 2016. ilus, graf
Artigo em Espanhol | IBECS | ID: ibc-157301

RESUMO

INTRODUCCIÓN: El único tratamiento curativo del cáncer de páncreas (CP) es la exéresis quirúrgica, pero debido a su presentación clínica tardía solo el 15-25% de los pacientes son candidatos a resección curativa. El objetivo de este trabajo, prospectivo y unicéntrico, es determinar la utilidad de la PET-TC preoperatoria en el diagnóstico precoz del CP, en su estadificación y en la detección de estadios precursores de la enfermedad en una serie de 139 pacientes sometidos a intervención quirúrgica con «intención curativa» y con el diagnóstico histológico de adenocarcinoma ductal. MÉTODOS: Hemos estudiado las características histopatológicas del CP y de las diferentes lesiones panIN en las piezas quirúrgicas de 139 pacientes sometidos a resección pancreática durante el periodo 2010-2014, comparando estos resultados con los datos preoperatorios de una tomografía computarizada multidetector con contraste trifásico (TCMD) y una PET-TC en la que la captación de glucosa fue determinada por el SUV, considerando malignidad por encima de 2,5. RESULTADOS: En nuestra serie, la sensibilidad de la PET-TC para el diagnóstico tumoral fue del 77,7% (108 de los 139 casos) versus el 75,5% (105 de los 139 casos) para la TCMD. Cuando combinamos este valor máximo del SUV tumoral con el SUV máximo de tejido pancreático normal de cada paciente, la sensibilidad diagnóstica de la PET-TC para el CP asciende al 94,9% (132 de los 139 casos). CONCLUSIÓN: Una combinación de los estudios del PET-TC en el tejido tumoral y no tumoral de cada paciente puede ser una herramienta diagnóstica muy útil no solo para el diagnóstico preoperatorio del CP, sino también para las lesiones panIN


INTRODUCTION: In pancreatic ductal adenocarcinoma (PDA), surgical resection is the only curative treatment, but due to its late clinical presentation only 15-25% patients are candidates for curative resection. The aim of this prospective, single-center study is to determine the diagnostic utility of preoperative PET-CT for early detection of PDA and early panIN lesions. METHODS: We studied the histopathological features of PDA and different panIN lesions in 139 surgical samples from patients undergoing pancreatic resection (from 2010-2014), comparing these results with preoperative PET-CT and MDCT study. For tumor diagnosis in PET-CT maximum standard SUV 2.5 was used. Pancreatic baseline SUVmax is the maximum uptake of the radiotracer 18-2FDG on the ROI curve determined for the area of the normal pancreas after pathological reassessment with areas not affected by tumours or preneoplastic lesions. Tumour Uptake Index is the ratio between the tumour SUVmax and pancreatic baseline SUVmax. RESULTS: Using an standard maximum SUV value of 2.5, PET-CT sensitivity was 77.7% (108 of the 139 cases) against 75.5% (105 of the 139 cases) of MDCT. But when we combined this value with maximum SUV of normal pancreatic tissue from each patient, PET-CT sensitivity improved its value to 94.9%. CONCLUSION: A combination of studies of PET-CT in tumor and non-tumor tissue of each patient might be a very useful diagnostic tool not only for preoperative diagnosis of PDA, but also for early panIN lesions


Assuntos
Humanos , Tomografia por Emissão de Pósitrons/métodos , Neoplasias Pancreáticas/diagnóstico , Pâncreas Exócrino/patologia , Pancreatectomia/métodos , Carcinoma Ductal Pancreático/diagnóstico , Fluordesoxiglucose F18 , Detecção Precoce de Câncer/métodos , Sensibilidade e Especificidade , Adenocarcinoma in Situ/cirurgia , Carcinoma Ductal Pancreático/cirurgia
3.
Clin. transl. oncol. (Print) ; 16(10): 865-878, oct. 2014.
Artigo em Inglês | IBECS | ID: ibc-127605

RESUMO

Exocrine pancreatic cancer (PC) is a very aggressive and heterogeneous tumor with several cellular signaling pathways implicated in its pathogenesis and maintenance. Several risk factors increase the risk of developing PC. Therapeutic strategies used are dictated by the extent of disease. Supportive treatment is critical because of the high frequency of symptoms. For localized disease, surgery followed by adjuvant gemcitabine is the standard. Neoadjuvant and new adjuvant chemotherapy regimens are being evaluated. Locally advanced disease should respond best guided by a multidisciplinary team. Various treatment options are appropriate such as chemotherapy alone or chemoradiotherapy with integration of rescue surgery if the tumor becomes resectable. In metastatic disease, chemotherapy should be reserved for patients with ECOG 0-1 using Folfirinox or gemcitabine plus nab-paclitaxel as the most recommended options. Several therapeutic strategies targeting unregulated pathways are under evaluation with an unmet need for biomarkers to guide management (AU)


No disponible


Assuntos
Humanos , Masculino , Feminino , Neoplasias Pancreáticas/diagnóstico , Neoplasias Pancreáticas/tratamento farmacológico , Biomarcadores Farmacológicos/análise , Biomarcadores Farmacológicos/metabolismo , Quimioterapia Adjuvante/instrumentação , Quimioterapia Adjuvante/métodos , Pâncreas Exócrino , Pâncreas Exócrino/patologia , Fatores de Risco , Biologia Molecular/métodos
4.
J. physiol. biochem ; 69(4): 897-908, dic. 2013.
Artigo em Inglês | IBECS | ID: ibc-121647

RESUMO

In the present work, we have evaluated the effect of an acute addition of melatonin on cholecystokinin octapeptide (CCK-8)-evoked Ca2+ signals and amylase secretion in mouse pancreatic acinar cells. For this purpose, freshly isolated mouse pancreatic acinar cells were loaded with fura-2 to study intracellular free Ca2+ concentration ([Ca2+]c). Amylase release and cell viability were studied employing colorimetric methods. Our results show that CCK-8 evoked a biphasic effect on amylase secretion, finding a maximum at a concentration of 0.1 nM and a reduction of secretion at higher concentrations. Pre-incubation of cells with melatonin (1 ìM–1 mM) significantly attenuated enzyme secretion in response to high concentrations of CCK-8. Stimulation of cells with 1 nM CCK-8 led to a transient increase in [Ca2+]c, followed by a decrease towards a constant level. In the presence of 1 mM melatonin, stimulation of cells with CCK-8 resulted in a smaller [Ca2+]c peak response, a faster rate of decay of [Ca2+]c and lower values for the steady state of [Ca2+]c, compared with the effect of CCK-8 alone. Melatonin also reduced the oscillatory pattern of Ca2+ mobilization evoked by a physiological concentration of CCK-8 (20 pM), and completely inhibited Ca2+mobilization induced by 10 pM CCK-8. On the other hand, Ca2+ entry from the extracellular space was not affected in the presence of melatonin. Finally, melatonin alone did not change cell viability. We conclude that melatonin, at concentrations higher than those found in blood, might regulate exocrine pancreatic function via modulation of Ca2+ signals (AU)


Assuntos
Animais , Ratos , Melatonina/farmacocinética , alfa-Amilases Pancreáticas , Cálcio/fisiologia , Colecistocinina/fisiologia , Células Acinares/fisiologia , Ilhotas Pancreáticas , Pâncreas Exócrino , Modelos Animais de Doenças , Substâncias Protetoras/farmacocinética
5.
Reumatol. clín. (Barc.) ; 7(2): 130-134, mar.-abr. 2011. tab
Artigo em Espanhol | IBECS | ID: ibc-86112

RESUMO

El síndrome de Sjögren (SS) es una enfermedad autoinmunitaria que afecta principalmente a las glándulas exocrinas, aunque puede ocasionar también manifestaciones extraglandulares. Dada la similitud anatómica, fisiológica y patológica del páncreas y las glándulas salivales, se ha descrito que el páncreas no está exento del daño producido por el síndrome de Sjögren. Por esta similitud, algunos autores han estudiado la influencia del SS en el páncreas analizando los cambios histopatológicos, evaluando la función pancreática endocrina y exocrina (medición de enzimas pancreáticas séricas, prueba de excreción de ácido N-benzoil-L-tirosil-para-aminobenzoico, medición de elastasa, lipasa o tripsina), por la detección de anticuerpos específicos para páncreas (Ac. anticonductos), o mediante la realización de colangiopancreatografía endoscópica retrógrada o estudios de imagen no invasivos (tomografía computarizada y ultrasonido). En el presente trabajo revisamos la literatura científica en relación con la prevalencia y el grado de afección pancreática en SS y discutimos sobre el diagnóstico diferencial con el síndrome linfoproliferativo multiorgánico(AU)


Sjögren's syndrome (SS) is an autoimmune disorder affecting primarily the exocrine glands, leading to keratoconjunctivitis sicca (KCS) and xerostomia, but that can also include extraglandular features1. Due the anatomical, physiological and pathological similarity between the pancreas and the salivary glands, it has been described that the pancreas it is not exempt from the damage produced by this syndrome. Some authors have assessed pancreatic involvement of SS by analyzing the histopathological changes, evaluating the pancreatic endocrine and exocrine function (serum pancreatic enzymes, elastase, lipase or trypsin determinations, N-benzoyl-L-tyrosyl-para-aminobenzoic acid excretion test, etc), searching specific pancreatic antibodies (antiductal) or performing endoscopic retrograde colangiopancreatography or noninvasive imaging studies such as computed tomography or ultrasound. Herein we review the literature regarding the prevalence and type of pancreatic involvement in the SS and we discuss the differential diagnosis with multiorganic Lymphoproliferative Syndrome(AU)


Assuntos
Humanos , Masculino , Feminino , Síndrome de Sjogren/complicações , Síndrome de Sjogren/diagnóstico , Síndrome de Sjogren/fisiopatologia , Insuficiência Pancreática Exócrina/complicações , Insuficiência Pancreática Exócrina/diagnóstico , Colangiopancreatografia por Ressonância Magnética , Doença de Mikulicz/complicações , Doença de Mikulicz/diagnóstico , Transtornos Linfoproliferativos/complicações , Transtornos Linfoproliferativos/diagnóstico , Síndrome de Sjogren/epidemiologia , Síndrome de Sjogren/terapia , Pâncreas Exócrino , Pâncreas Exócrino/patologia , Pâncreas Exócrino , Endoscopia/tendências , Endoscopia , /instrumentação , /métodos
6.
J. physiol. biochem ; 64(3): 243-258, jul.-sept. 2008. ilus
Artigo em Inglês | IBECS | ID: ibc-61829

RESUMO

The pancreatic ductal tree conveys enzymatic acinar products to the duodenumand secretes the fluid and ionic components of pancreatic juice. The physiology ofpancreatic duct cells has been widely studied, but many questions are still unansweredconcerning their mechanisms of ionic transport. Differences in the transportmechanisms operating in the ductal epithelium has been described both among differentspecies and in the different regions of the ductal tree. In this review we summarizethe methods developed to study pancreatic duct secretion both in vivo and invitro, the different mechanisms of ionic transport that have been reported to date inthe basolateral and luminal membranes of pancreatic ductal cells and the regulationof pancreatic duct secretion by nervous, endocrine and paracrine influences(AU)


No disponible


Assuntos
Animais , Transporte de Íons/fisiologia , Pâncreas Exócrino/fisiologia , Ductos Pancreáticos , Técnicas de Cultura de Células/métodos , Membrana Celular/fisiologia , Hormônios Gastrointestinais/fisiologia , Ductos Pancreáticos/fisiologia , Comunicação Parácrina/fisiologia , Secretina/fisiologia , Bombas de Íon/fisiologia , Ductos Pancreáticos/citologia , Ductos Pancreáticos/inervação , Comunicação Parácrina , Perfusão/métodos , Sistema Nervoso Periférico/fisiologia , Punções/métodos , Secretina/metabolismo , Modelos Animais
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