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1.
J Multidiscip Healthc ; 14: 1311-1324, 2021.
Artículo en Inglés | MEDLINE | ID: mdl-34113119

RESUMEN

BACKGROUND: Patient-centeredness is essential in complex oncological multidisciplinary team decision-making. Improvement seems to be needed, while there is a lack of knowledge about health care providers' needs for improvement. OBJECTIVE: To explore multidisciplinary team members' perspectives on the need to improve patient-centeredness in complex decision-making, and subsequently the strategies to enhance it. METHODS: This was a qualitative descriptive interview study. The participants were twenty-four professionals who attended multidisciplinary cancer team meetings weekly. The setting was five multidisciplinary teams (gastrointestinal, gynecological, urological, head and neck, and hematological cancer) in a Dutch academic hospital. Data were collected by semi-structured interviews and were analyzed with a combination of inductive and deductive content analysis. RESULTS: The participants voiced the need for additional information (patient-centered information, patients's needs and preferences, individualized medical information) during the multidisciplinary team meeting, to be more patient-centered in the decision-making conversation with the patient following the meeting, and for more information following the meeting to support patient-centeredness. The strategies, which mostly originated from the needs, were categorized as organization, decision-making, and communication. The most prominent strategies were those aimed at collecting and using patient-centered information, and to facilitate the decision-making conversation with the patient following the multidisciplinary team meeting. CONCLUSION: Our findings highlighted the need to improve patient-centeredness in oncological multidisciplinary teams and provided a comprehensive overview of strategies for improvement, supported by multidisciplinary team members. These strategies emphasize involvement of patients throughout the continuous process of decision-making for patients with cancer. These strategies may be implemented in other oncological multidisciplinary teams, taking in mind the local needs. Future research may help to prioritize the strategies and to determine and evaluate the effect on endpoints, like patient or professional satisfaction, shared decision-making, and on the decision that was made.

2.
Reprod Sci ; 23(1): 11-23, 2016 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-26335175

RESUMEN

Endometriosis is an estrogen (ER)-dependent gynecological disease caused by the growth of endometrial tissue at extrauterine sites. Current endocrine therapies address the estrogenic aspect of disease and offer some relief from pain but are associated with significant side effects. Immune dysfunction is also widely believed to be an underlying contributor to the pathogenesis of this disease. This study evaluated an inhibitor of c-Jun N-terminal kinase, bentamapimod (AS602801), which interrupts immune pathways, in 2 rodent endometriosis models. Treatment of nude mice bearing xenografts biopsied from women with endometriosis (BWE) with 30 mg/kg AS602801 caused 29% regression of lesion. Medroxyprogesterone acetate (MPA) or progesterone (PR) alone did not cause regression of BWE lesions, but combining 10 mg/kg AS602801 with MPA caused 38% lesion regression. In human endometrial organ cultures (from healthy women), treatment with AS602801 or MPA reduced matrix metalloproteinase-3 (MMP-3) release into culture medium. In organ cultures established with BWE, PR or MPA failed to inhibit MMP-3 secretion, whereas AS602801 alone or MPA + AS602801 suppressed MMP-3 production. In an autologous rat endometriosis model, AS602801 caused 48% regression of lesions compared to GnRH antagonist Antide (84%). AS602801 reduced inflammatory cytokines in endometriotic lesions, while levels of cytokines in ipsilateral horns were unaffected. Furthermore, AS602801 enhanced natural killer cell activity, without apparent negative effects on uterus. These results indicate that bentamapimod induced regression of endometriotic lesions in endometriosis rodent animal models without suppressing ER action. c-Jun N-terminal kinase inhibition mediated a comprehensive reduction in cytokine secretion and moreover was able to overcome PR resistance.


Asunto(s)
Benzotiazoles/uso terapéutico , Endometriosis/tratamiento farmacológico , Endometrio/efectos de los fármacos , Inhibidores Enzimáticos/uso terapéutico , Proteínas Quinasas JNK Activadas por Mitógenos/antagonistas & inhibidores , Pirimidinas/uso terapéutico , Adulto , Animales , Benzotiazoles/farmacología , Citocinas/metabolismo , Modelos Animales de Enfermedad , Endometriosis/metabolismo , Endometrio/metabolismo , Inhibidores Enzimáticos/farmacología , Femenino , Humanos , Células Asesinas Naturales/efectos de los fármacos , Células Asesinas Naturales/metabolismo , Sistema de Señalización de MAP Quinasas/efectos de los fármacos , Metaloproteinasa 3 de la Matriz/metabolismo , Acetato de Medroxiprogesterona/farmacología , Acetato de Medroxiprogesterona/uso terapéutico , Ratones , Ratones Desnudos , Progesterona/farmacología , Progesterona/uso terapéutico , Pirimidinas/farmacología , Ratas
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