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1.
Diabetes Obes Metab ; 18 Suppl 1: 63-70, 2016 09.
Artigo em Inglês | MEDLINE | ID: mdl-27615133

RESUMO

Pregnancy in placental mammals places unique demands on the insulin-producing ß-cells in the pancreatic islets of Langerhans. The pancreas anticipates the increase in insulin resistance that occurs late in pregnancy by increasing ß-cell numbers and function earlier in pregnancy. In rodents, this ß-cell expansion depends on secreted placental lactogens that signal through the prolactin receptor. Then at the end of pregnancy, the ß-cell population contracts back to its pre-pregnancy size. In the current review, we focus on how glucose metabolism changes during pregnancy, how ß-cells anticipate these changes through their response to lactogens and what molecular mechanisms guide the adaptive compensation. In addition, we summarize current knowledge of ß-cell adaptation during human pregnancy and what happens when adaptation fails and gestational diabetes ensues. A better understanding of human ß-cell adaptation to pregnancy would benefit efforts to predict, prevent and treat gestational diabetes.


Assuntos
Adaptação Fisiológica , Proliferação de Células , Glucose/metabolismo , Células Secretoras de Insulina/metabolismo , Insulina/metabolismo , Gravidez/metabolismo , Animais , Diabetes Gestacional/metabolismo , Feminino , Humanos , Resistência à Insulina , Secreção de Insulina , Células Secretoras de Insulina/citologia , Camundongos , Lactogênio Placentário/metabolismo , Período Pós-Parto , Ratos , Serotonina/metabolismo
2.
Diabetes Obes Metab ; 18 Suppl 1: 144-51, 2016 09.
Artigo em Inglês | MEDLINE | ID: mdl-27615144

RESUMO

Creating an abundant source of ß(-like)-cells has been a major goal in diabetes research for many decades. The concept of cell plasticity has inspired many strategies towards regenerative medicine, but its successes have been limited until very recently. Today, most cell types in the pancreas are considered candidates for the generation of ß(-like)-cells through transdifferentiation. While ß(-like)-cells that are in vitro differentiated from human embryonic stem cells are already being grafted in patients, ß(-like)-cells generated by transdifferentiation are not yet ready for clinical application. These cells would however offer several advantages over the current ß(-like)-cells generated by directed differentiation, especially concerning safety issues. In addition, perfect control of the transdifferentiation efficiency would through targeted drug delivery support a non-invasive cell therapy for diabetes. Lastly, focusing on the exocrine pancreas as prime candidate makes sense in view of their abundance and high plasticity. Keeping these hopeful perspectives in mind, it is worth to continue focused research on the mechanisms that control transdifferentiation from pancreas exocrine to ß-cells.


Assuntos
Plasticidade Celular , Transdiferenciação Celular , Técnicas de Reprogramação Celular/métodos , Diabetes Mellitus/terapia , Células Secretoras de Insulina/citologia , Pâncreas Exócrino/citologia , Terapia Baseada em Transplante de Células e Tecidos/métodos , Humanos , Células Secretoras de Insulina/transplante
3.
Cell Death Dis ; 7(6): e2272, 2016 06 23.
Artigo em Inglês | MEDLINE | ID: mdl-27336716

RESUMO

Partial pancreatic duct ligation (PDL) of mouse pancreas induces a doubling of the ß-cell mass mainly through proliferation of pre-existing and newly formed ß-cells. The molecular mechanism governing this process is still largely unknown. Given the inflammatory nature of PDL and inflammation-induced signaling via the signal transducer and activator of transcription 3 (STAT3), the activation and the role of STAT3 in PDL-induced ß-cell proliferation were investigated. Duct ligation stimulates the expression of several cytokines that can act as ligands inducing STAT3 signaling and phosphorylation in ß-cells. ß-Cell cycling increased by conditional ß-cell-specific Stat3 knockout and decreased by STAT3 activation through administration of interleukin-6. In addition, the level of DNA damage in ß-cells of PDL pancreas increased after deletion of Stat3. These data indicate a role for STAT3 in maintaining a steady state in the ß-cell, by modulating its cell cycle and protection from DNA damage.


Assuntos
Ciclo Celular , Citoproteção , Dano ao DNA , Células Secretoras de Insulina/metabolismo , Células Secretoras de Insulina/patologia , Fator de Transcrição STAT3/metabolismo , Animais , Ciclo Celular/efeitos dos fármacos , Citocinas/metabolismo , Citoproteção/efeitos dos fármacos , Células Secretoras de Insulina/efeitos dos fármacos , Peptídeos e Proteínas de Sinalização Intercelular/metabolismo , Interleucina-6/farmacologia , Antígeno Ki-67/metabolismo , Ligadura , Masculino , Camundongos Endogâmicos BALB C , Camundongos Knockout , Ductos Pancreáticos/efeitos dos fármacos , Ductos Pancreáticos/patologia , Proteínas Recombinantes/farmacologia
4.
Cell Death Differ ; 22(7): 1117-30, 2015 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-25476775

RESUMO

Rodent acinar cells exhibit a remarkable plasticity as they can transdifferentiate to duct-, hepatocyte- and islet ß-like cells. We evaluated whether exocrine cells from adult human pancreas can similarly respond to proendocrine stimuli. Exocrine cells from adult human pancreas were transduced directly with lentiviruses expressing activated MAPK (mitogen-activated protein kinase) and STAT3 (signal transducer and activator of transcription 3) and cultured as monolayers or as 3D structures. Expression of STAT3 and MAPK in human exocrine cells activated expression of the proendocrine factor neurogenin 3 in 50% to 80% of transduced exocrine cells. However, the number of insulin-positive cells increased only in the exocrine cells grown initially in suspension before 3D culture. Lineage tracing identified human acinar cells as the source of Ngn3- and insulin-expressing cells. Long-term engraftment into immunocompromised mice increased the efficiency of reprogramming to insulin-positive cells. Our data demonstrate that exocrine cells from human pancreas can be reprogrammed to transplantable insulin-producing cells that acquire functionality. Given the large number of exocrine cells in a donor pancreas, this approach presents a novel strategy to expand cell therapy in type 1 diabetes.


Assuntos
Transdiferenciação Celular/genética , Transplante de Células , Células Secretoras de Insulina/metabolismo , Proteínas Quinases Ativadas por Mitógeno/genética , Pâncreas Exócrino/citologia , Pâncreas Exócrino/metabolismo , Fator de Transcrição STAT3/genética , Animais , Fatores de Transcrição Hélice-Alça-Hélice Básicos , Humanos , Células Secretoras de Insulina/transplante , Camundongos , Proteínas do Tecido Nervoso , Transdução Genética , Regulação para Cima
5.
Cell Death Dis ; 4: e523, 2013 Mar 07.
Artigo em Inglês | MEDLINE | ID: mdl-23470530

RESUMO

We previously showed that injury by partial duct ligation (PDL) in adult mouse pancreas activates Neurogenin 3 (Ngn3)(+) progenitor cells that can differentiate to ß cells ex vivo. Here we evaluate the role of Ngn3(+) cells in ß cell expansion in situ. PDL not only induced doubling of the ß cell volume but also increased the total number of islets. ß cells proliferated without extended delay (the so-called 'refractory' period), their proliferation potential was highest in small islets, and 86% of the ß cell expansion was attributable to proliferation of pre-existing ß cells. At sufficiently high Ngn3 expression level, upto 14% of all ß cells and 40% of small islet ß cells derived from non-ß cells. Moreover, ß cell proliferation was blunted by a selective ablation of Ngn3(+) cells but not by conditional knockout of Ngn3 in pre-existing ß cells supporting a key role for Ngn3(+) insulin(-) cells in ß cell proliferation and expansion. We conclude that Ngn3(+) cell-dependent proliferation of pre-existing and newly-formed ß cells as well as reprogramming of non-ß cells contribute to in vivo ß cell expansion in the injured pancreas of adult mice.


Assuntos
Fatores de Transcrição Hélice-Alça-Hélice Básicos/metabolismo , Células Secretoras de Insulina/fisiologia , Proteínas do Tecido Nervoso/metabolismo , Pâncreas/metabolismo , Animais , Fatores de Transcrição Hélice-Alça-Hélice Básicos/genética , Proliferação de Células , Tamanho Celular , Insulina/metabolismo , Células Secretoras de Insulina/citologia , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Proteínas do Tecido Nervoso/genética , Pâncreas/lesões , Pâncreas/patologia , Regeneração
6.
Diabetologia ; 55(4): 1024-34, 2012 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-22237687

RESUMO

AIMS/HYPOTHESIS: Transdifferentiation of pancreatic exocrine cells into insulin-producing beta cells may represent an important alternative to islets required for diabetes cell therapy. Rat pancreatic acinar cells are known to transdifferentiate into functional beta cells, with recapitulation of several pancreas developmental features. Considering the inhibitory functions of hedgehog signalling in early and mid-stage pancreatic development, we questioned whether it also operates in transdifferentiating acinar cells and whether its modulation would influence postnatal beta cell neogenesis in vitro. METHODS: Rat exocrine cells were precultured in suspension for 4 days and then incubated with EGF and leukaemia inhibitory factor (LIF) for 72 h. The hedgehog signalling pathway was modulated during this, and its effects analysed by RT-PCR, immunocytochemistry and western blot. RESULTS: Our data indicate induction of Dhh and Ihh, but not Shh, expression during acinar cell culture, resulting in activation of hedgehog targets (Ptc1, Gli1). Exposure of the metaplastic cells to EGF and LIF induced beta cell differentiation without affecting endogenous hedgehog activity. Whereas blocking endogenous hedgehog only slightly increased beta cell neogenesis, exposure to embryoid body-conditioned medium activated hedgehog signalling as well as other pathways such as Notch, resulting in severe blockade of beta cell neogenesis. Interestingly, this effect was partially rescued by treatment with the hedgehog inhibitor, 3-keto-N-(aminoethyl-aminocaproyl-dihydrocinnamoyl)-cyclopamine (KAAD-cyclopamine), alone. CONCLUSIONS/INTERPRETATION: We report here Dhh/Ihh-dependent activation of hedgehog targets during pancreatic exocrine cell metaplasia in vitro and a persistent inhibitory function of hedgehog signalling in a model of postnatal beta cell differentiation.


Assuntos
Células Acinares/metabolismo , Transdiferenciação Celular/fisiologia , Proteínas Hedgehog/metabolismo , Pâncreas Exócrino/metabolismo , Transdução de Sinais/fisiologia , Células Acinares/efeitos dos fármacos , Animais , Transdiferenciação Celular/efeitos dos fármacos , Fator de Crescimento Epidérmico/farmacologia , Células Secretoras de Insulina/efeitos dos fármacos , Células Secretoras de Insulina/metabolismo , Fatores de Transcrição Kruppel-Like/metabolismo , Fator Inibidor de Leucemia/farmacologia , Camundongos , Pâncreas Exócrino/efeitos dos fármacos , Receptores Patched , Receptor Patched-1 , Ratos , Ratos Wistar , Receptores de Superfície Celular/metabolismo , Transdução de Sinais/efeitos dos fármacos , Proteína GLI1 em Dedos de Zinco
7.
Eur J Gynaecol Oncol ; 29(5): 535-7, 2008.
Artigo em Inglês | MEDLINE | ID: mdl-19051830

RESUMO

UNLABELLED: Small cell ovarian tumors are rare and highly malignant, occurring mainly in young patients. Early mortality is high due to the lack of an effective treatment. The first adjuvant therapy is usually chemotherapy. CASE: During laparotomy for renal transplant in a 17-year-old girl, the right ovary exhibited a suspicious mass, whose pathological diagnosis was Stage 1A small cell ovarian tumor. Prognosis was poor (young age, hypercalcemia, tumor >10 cm, and presence of large cells). Since chemotherapy is contraindicated for dialysed patients, only radiotherapy was given. The patient is still alive and disease-free ten years after diagnosis. CONCLUSION: This is the first case with a poor prognosis reported in the literature that has been successfully cured by surgery plus adjuvant radiotherapy only.


Assuntos
Carcinoma de Células Pequenas/terapia , Neoplasias Ovarianas/terapia , Adolescente , Intervalo Livre de Doença , Feminino , Humanos , Radioterapia Adjuvante
8.
Diabetes Obes Metab ; 10 Suppl 4: 170-8, 2008 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-18834444

RESUMO

A major goal of research aiming at improving islet cell replacement therapy is to find the most suitable progenitor cell type from which functional beta-cells can be generated in large numbers. Many possibilities have been raised, including beta-cells themselves, embryonic or adult stem cells and reprogramming of other cell types. Some of these progenitor types may be active or reside in a dormant state in adults in vivo, while others can be rather considered to be products of tissue engineering in vitro. Starting from the available pancreas organs from cadaveric donors, an attractive possibility is to reprogram acinar exocrine cells into beta-cells. Indeed, acinar cells isolated from adult rats display a pronounced plasticity in culture. After an initial step of dedifferentiation, they can be redirected to the beta-cell phenotype by adding agonists of the JAK2/STAT3 signalling pathway to the medium (epidermal growth factor and leukaemia inhibitory factor). The acinar cells that undergo exocrine-to-endocrine transdifferentiation first need to re-express neurogenin-3 and then need to escape inhibition by Notch signalling. The insulin-expressing cells that are generated in this way are glucose-regulated and can normalize glycaemia after transplantation into diabetic immunocompromised mice. It will now be important to translate these findings to human cells.


Assuntos
Diabetes Mellitus Tipo 1/fisiopatologia , Células Secretoras de Insulina/citologia , Transplante das Ilhotas Pancreáticas/métodos , Pâncreas Exócrino/citologia , Regeneração/fisiologia , Células-Tronco/citologia , Animais , Pesquisa Biomédica , Diferenciação Celular/fisiologia , Feminino , Humanos , Insulina/metabolismo , Ilhotas Pancreáticas/citologia , Ilhotas Pancreáticas/metabolismo , Ilhotas Pancreáticas/fisiologia , Masculino , Camundongos , Pâncreas Exócrino/metabolismo , Transdução de Sinais/fisiologia , Células-Tronco/metabolismo , Células-Tronco/fisiologia
9.
Cell Death Differ ; 13(11): 1892-9, 2006 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-16514419

RESUMO

The basic helix-loop-helix protein Neurogenin3 specifies precursor cells of the endocrine pancreas during embryonic development, and is thought to be absent postnatally. We have studied Ngn3 expression during in vitro generation of beta-cells from adult rat exocrine pancreas tissue treated with epidermal growth factor and leukaemia inhibitory factor. This treatment induced a transient expression of both Ngn3 and its upstream activator hepatocyte nuclear factor 6. Inhibition of EGF and LIF signalling by pharmacological antagonists of the JAK2/STAT3 pathway, or knockdown of Ngn3 by RNA interference prevented the generation of new insulin-positive cells. This study demonstrates that in vitro growth factor stimulation can induce recapitulation of an embryonic endocrine differentiation pathway in adult dedifferentiated exocrine cells. This could prove to be important for understanding the mechanism of beta-cell regeneration and for therapeutic ex vivo neogenesis of beta cells.


Assuntos
Fatores de Transcrição Hélice-Alça-Hélice Básicos/metabolismo , Células Secretoras de Insulina/citologia , Células Secretoras de Insulina/metabolismo , Janus Quinase 2/metabolismo , Proteínas do Tecido Nervoso/metabolismo , Fator de Transcrição STAT3/metabolismo , Transdução de Sinais , Animais , Animais Recém-Nascidos , Fatores de Transcrição Hélice-Alça-Hélice Básicos/genética , Células Cultivadas , Perfilação da Expressão Gênica , Inativação Gênica , Substâncias de Crescimento/farmacologia , Fator 6 Nuclear de Hepatócito/genética , Humanos , Células Secretoras de Insulina/efeitos dos fármacos , Lipase/metabolismo , Masculino , Modelos Animais , Proteínas do Tecido Nervoso/genética , Niacinamida/farmacologia , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Ratos , Ratos Wistar , Transdução de Sinais/efeitos dos fármacos , Regulação para Cima/efeitos dos fármacos
10.
Diabetologia ; 49(1): 108-16, 2006 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-16369772

RESUMO

AIMS/HYPOTHESIS: It was recently reported that culturing adult exocrine cells in the presence of epidermal growth factor and leukaemia inhibitory factor (LIF) resulted in their transdifferentiation into endocrine beta cells. The aim of this study was to examine the expression and function of LIF in the pancreas. MATERIALS AND METHODS: We studied the expression of LIF and its receptor components, LIF-receptor-beta and gp130, by immunohistochemistry, western blotting and RT-PCR in normal rat pancreas, pancreas with duct ligation-induced islet neogenesis, and in pancreatic cell cultures. Isolated duct fragments were cultured in the presence of LIF and a janus kinase 2 (JAK2) inhibitor. RESULTS: LIF was detected by immunohistochemistry, western blot and RT-PCR in the ducts of the normal pancreas. Both LIF-receptor-beta and gp130 were detected by RT-PCR in the pancreas. Immunostaining revealed gp130 exclusively in the ducts and centro-acinar cells. After duct ligation-induced tissue injury, upregulation of LIF and its receptor occurred in rat pancreas. Metaplastic exocrine cells also started to express LIF and this was increased after alloxan treatment. Signalling via LIF-receptor-beta/gp130 involves the JAK/signal transducer and activator of transcription (STAT) pathway. LIF induced increased activation of STAT3 in pancreatic cells. In isolated duct fragments, addition of LIF resulted in a significant increase in duct cell proliferation, while a specific inhibitor of the JAK/STAT signalling pathway inhibited proliferation. CONCLUSION/INTERPRETATION: Our observations show that LIF and its receptor are expressed in cells from pancreatic ducts. The cytokine plays a role in pancreatic physiology, controls duct cell proliferation and is involved in repair processes following pancreatic injury.


Assuntos
Interleucina-6/genética , Pâncreas/fisiologia , Receptores de Citocinas/genética , Animais , Imuno-Histoquímica , Insulina/análise , Fator Inibidor de Leucemia , Subunidade alfa de Receptor de Fator Inibidor de Leucemia , Masculino , Ductos Pancreáticos/fisiologia , Ratos , Ratos Wistar , Receptores de OSM-LIF , Valores de Referência , Regeneração , Reação em Cadeia da Polimerase Via Transcriptase Reversa
11.
Cancer Radiother ; 9(3): 183-6, 2005 May.
Artigo em Francês | MEDLINE | ID: mdl-16023045

RESUMO

Ovarian metastasis as first dissemination site of a lung adenocarcinoma has not been described in the literature. We report the case of a 61-year-old woman who had a pneumectomy for a centrally located lung adenocarcinoma, which was discovered on a routine chest X-Ray. During the follow-up, a Positron Emission Tomography (PET)-Scan showed a hypercaptation in the pelvic region. Abdominal CT-scan confirmed the presence of a mass which was compatible with a primary ovarian tumor. The patient underwent a hysterectomy and bilateral salpingo-oophorectomy. Pathology reported an adenocarcinoma. Immunohistochemical staining revealed cells expression for Thyroid Transcription Factor 1 (TTF-1), cytokeratin 7 (CK-7) and focally cytokeratin 20 (CK-20). Clinical course, pathological and immunohistochemical data concluded to the diagnosis of ovarian metastasis of the lung adenocarcinoma. In conclusion, in the differential diagnosis of an ovarian metastasis, clinicians should not forget the lung as primary site since epidemiologic data of lung cancer in women show progressive incidence.


Assuntos
Adenocarcinoma/secundário , Carcinoma Pulmonar de Células não Pequenas/secundário , Neoplasias Pulmonares/patologia , Neoplasias Ovarianas/secundário , Adenocarcinoma/diagnóstico , Carcinoma Pulmonar de Células não Pequenas/diagnóstico , Diagnóstico Diferencial , Feminino , Humanos , Imuno-Histoquímica , Neoplasias Pulmonares/diagnóstico , Pessoa de Meia-Idade , Neoplasias Ovarianas/diagnóstico , Pneumonectomia , Tomografia por Emissão de Pósitrons
12.
Diabetologia ; 48(1): 49-57, 2005 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-15616797

RESUMO

AIMS/HYPOTHESIS: Transplantation of insulin-producing beta cells from donors can cure diabetes, but they are available in insufficient quantities. In this study, we investigated the possibility of generating insulin-producing cells from adult rat exocrine cells cultured in the presence of growth factors. METHODS: Rat exocrine pancreatic cells were isolated and treated in vitro with epidermal growth factor (EGF) and leukaemia inhibitory factor (LIF). Analysis was performed by immunocytochemistry, DNA measurement and radioimmunoassay. Cells were transplanted to alloxan-treated (70 mg/kg) nude mice and glycaemia was monitored for 21 days. Nephrectomy was performed on day 15. RESULTS: In a 3-day culture period, addition of LIF plus EGF to the medium resulted in an 11-fold increase of the beta cell mass. This could not be attributed to the very low mitotic activity of contaminating beta cells. Furthermore, when contaminating beta cells were initially destroyed with alloxan, this effect was even more pronounced. The newly formed cells secreted insulin in response to glucose and were immunoreactive for C-peptide-I, Pdx-1 and GLUT-2, which are characteristics of mature beta cells. Electron microscopy showed that they also contained insulin-immunoreactive secretory granules. Some insulin-positive cells were immunoreactive for amylase and cytokeratin-20, or were binucleated, which are characteristics of exocrine cells. The cells were able to restore normoglycaemia when transplanted to alloxan-diabetic mice, and hyperglycaemia recurred upon removal of the graft. CONCLUSIONS/INTERPRETATION: Our study shows that functional beta cells can be generated from exocrine tissue by transdifferentiation and thereby may offer a new perspective for beta cell therapy.


Assuntos
Insulina/metabolismo , Ilhotas Pancreáticas/fisiologia , Animais , Separação Celular , Fator de Crescimento Epidérmico/farmacologia , Glucose/farmacologia , Secreção de Insulina , Interleucina-6/farmacologia , Ilhotas Pancreáticas/citologia , Ilhotas Pancreáticas/efeitos dos fármacos , Ilhotas Pancreáticas/metabolismo , Fator Inibidor de Leucemia , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Nus , Ratos , Ratos Wistar
13.
J Gynecol Obstet Biol Reprod (Paris) ; 33(7): 649-51, 2004 Nov.
Artigo em Francês | MEDLINE | ID: mdl-15550884

RESUMO

We report the first case of detection of sentinel node in a 54 year-old woman presenting an adenocarcinoma of Bartholin's gland. Primary carcinoma of Bartholin's gland is rare and represents 2-7% of vulvar malignant lesions; this could explain the lack of consensus about treatment. The best attitude could be vulvectomy and inguinal lymphadenectomy. Pelvic lymphadenectomy is not required when no pelvic sentinel node is observed or when no metastatic inguinal node can be detected.


Assuntos
Adenocarcinoma/diagnóstico , Glândulas Vestibulares Maiores/patologia , Biópsia de Linfonodo Sentinela , Neoplasias Vulvares/diagnóstico , Adenocarcinoma/patologia , Adenocarcinoma/cirurgia , Glândulas Vestibulares Maiores/cirurgia , Feminino , Virilha , Humanos , Excisão de Linfonodo , Pessoa de Meia-Idade , Pelve , Resultado do Tratamento , Vulva/cirurgia , Neoplasias Vulvares/patologia , Neoplasias Vulvares/cirurgia
14.
Artigo em Francês | MEDLINE | ID: mdl-12592184

RESUMO

Spontaneous rupture of utero-ovarian veins occurring during pregnancy or the peripartal period is generally considered to be a medical curiosity (approximately 100 reported cases) rarely mentioned in obstetric textbooks. It is nevertheless a dramatic cause of maternal and /or fetal mortality. The available statistics are the following: 60% of the cases are directly related to labor and 50% occur in primiparas; when the rupture is associated with labor, mortality is 40%. Occurring outside of labor, mortality rate is approximatively 10%. The perinatal mortality remains high at 30%; in 75% of the cases, the broad ligament is the site of rupture (in many cases, the site of rupture is not found, at laparotomy or autopsy). We report the case of a patient who developed ovarian vein rupture on the 3rd postpartum day.


Assuntos
Ovário/irrigação sanguínea , Hemorragia Pós-Parto/diagnóstico , Útero/irrigação sanguínea , Adulto , Feminino , Humanos , Hemorragia Pós-Parto/cirurgia , Gravidez , Ruptura Espontânea/diagnóstico , Ruptura Espontânea/cirurgia , Resultado do Tratamento , Veias
15.
Rev Med Brux ; 16(4): 214-5, 1995.
Artigo em Francês | MEDLINE | ID: mdl-7481226

RESUMO

A detailed senologic evaluation with complete clinical examination, (color Doppler) echography, comparative mammography and cytology or microbiopsy can avoid surgery in case of a post-traumatic fat necrosis, a Mondor Syndrome, an infectious mastitis or a ductal ecstasy with nipple discharge. Actually we have still difficulties to interpret non palpable breast lesions and to supervise operated and radiated breasts.


Assuntos
Doenças Mamárias/diagnóstico , Neoplasias da Mama/diagnóstico , Biomarcadores Tumorais/isolamento & purificação , Biópsia por Agulha , Neoplasias da Mama/cirurgia , Diagnóstico Diferencial , Diagnóstico por Imagem , Feminino , Humanos , Mamografia , Mastectomia/métodos
17.
Artigo em Francês | MEDLINE | ID: mdl-3598099

RESUMO

Gynaecological types of pain in high-powered sportswomen can be of traumatic origin (bony, muscular or cartilaginous) in the region around the pubis. A case of vaginal pain which proved to be due to adductor tendinitis in the hip in a long distance walker is described. A review of the differential diagnosis of gynaecological pain that can occur in sportswomen is carried out. These consist of instability in the symphysis of the pubis as well as muscular lesions of the abdominal muscles of the hip adductors and of the ilio-psoas muscles. In addition, stress fractures of the pubic rami as well as inflammation of the symphysis due to stress, and pubic osteomyelitis are described.


Assuntos
Dor/etiologia , Esportes , Tendinopatia/complicações , Doenças Vaginais/etiologia , Feminino , Humanos , Pessoa de Meia-Idade , Tendinopatia/etiologia
18.
J Clin Endocrinol Metab ; 60(6): 1250-2, 1985 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-3998069

RESUMO

The response of plasma PRL to exercise, as performed on a bicycle ergometer under conditions below and above the anaerobic threshold, was studied in 10 normal young men. One hour of submaximal work against a workload at which blood lactic acid remained below 4 mmol/liter (anaerobic threshold) was accompanied by a slight decrease in plasma PRL levels, similar to the changes occurring under control conditions in the same subjects. However, during graded maximal ergometric exercise until exhaustion, plasma PRL rose promptly and significantly (P less than 0.05) when the anaerobic threshold was reached. These data suggest that PRL levels increase provided that the intensity of exercise is such that the anaerobic threshold is reached.


Assuntos
Anaerobiose , Metabolismo , Esforço Físico , Prolactina/sangue , Adulto , Fenômenos Químicos , Química , Humanos , Masculino , Resistência Física
19.
Fertil Steril ; 43(4): 628-31, 1985 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-3987929

RESUMO

The effects of Pergolide, a potent dopamine agonist, on exercise-induced plasma prolactin (PRL) changes were studied in normal men. Exercises consisted of a graded bicycle ergometer test and of a 20-km endurance run. In both circumstances, treatment with Pergolide, when compared with placebo or control values, resulted in a significant suppression of basal PRL (P less than 0.001) as well as of exercise-induced PRL increase (P less than 0.01). From these experiments it was concluded that augmented levels of PRL in plasma, as seen during or after muscular exercise, are caused by increased pituitary secretion, rather than decreased elimination.


Assuntos
Antagonistas de Dopamina , Ergolinas/farmacologia , Esforço Físico , Prolactina/metabolismo , Adulto , Hematócrito , Humanos , Masculino , Pessoa de Meia-Idade , Pergolida , Adeno-Hipófise/metabolismo , Corrida
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