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1.
Nagoya J Med Sci ; 80(4): 465-473, 2018 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-30587861

RESUMEN

To minimise the global burden of diabetes, the awareness of appropriate intervention methods for diabetes education and practice is essential. This project is the first international interprofessional education (IIPE) for the awareness of diabetes, with a focus on patient-centred care wherein three medical and four pharmacy students from Japan and one medical, two pharmacy, two nutrition and one occupational therapy (OT) student from Scotland participated. We described IIPE effects using interdisciplinary education perception scale (IEPS) before and after the programme among Scottish and Japanese students. University of Aberdeen/ Robert Gordon University and Nagoya University developed and established a shared online platform that provided knowledge to students on diabetes in both languages. We developed a case-based scenario that reflected diabetes care in each country using a standardised patient (SP). Lastly, a student-led live webinar was conducted on 14 November 2014 (the World Diabetes Day) to discuss and exchange care methods for SP. Each participating national team presented their care plan and all students discussed the diabetic care plan online. Both Japanese and Scottish teams were able to accurately assess the patient's condition and empathise with the SP. In conclusion, all participants learned that interprofessional collaboration was clearly required for diabetes management focused on patient-centred care. All participants appreciated the differences in the approach of the two countries involved because of the cultural- and health related differences. This programme was significant in raising awareness regarding the need for international interprofessional intervention on diabetes towards developing a model for live webinar IIPE.


Asunto(s)
Diabetes Mellitus , Estudios Interdisciplinarios , Atención Dirigida al Paciente/métodos , Humanos , Japón , Grupo de Atención al Paciente , Escocia , Difusión por la Web como Asunto
2.
J Bodyw Mov Ther ; 22(2): 328-332, 2018 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-29861227

RESUMEN

BACKGROUND: Myofascial pain syndrome (MPS) is a condition that involves skeletal muscles. It is caused by overload or disuse of muscles and is characterized by extreme tenderness in the muscles with taut bands. Treatment for MPS is different from that for cancer-related pain. Cancer patients have many factors that cause restriction of body movement and posture. Although cancer patients appear to demonstrate risk factors for MPS, its prevalence has not been reported in patients with incurable cancer. This study was conducted to investigate the prevalence of MPS in patients with incurable cancer. METHODS: A retrospective chart review. The data for patients with incurable cancer who received palliative care at our department between September 2015 and March 2016 were investigated. We examined the prevalence of MPS, which was diagnosed on the basis of the Rivers criteria (RC) and Simons criteria (SC). We also examined the following factors associated with MPS: performance status (PS), use of medical devices, and primary cancer sites. The primary outcome was the prevalence of MPS based on RC. Secondary outcomes included the prevalence of MPS based on SC and the relationship between MPS and either PS or medical devices. RESULTS: Thirty-four patients with incurable cancer were identified. MPS based on RC or SC was detected in 10 (29%) and 20 (59%) patients, respectively. Twenty-two of 34 patients who complained of pain, 10 (45%) had MPS based on RC and 20 (90%) had MPS based on SC. Age and central venous port were risk factors for MPS by multivariate analysis. CONCLUSION: A very high prevalence of MPS was detected in our study population. MPS should be considered when patients with incurable cancer complain of pain.

3.
Jpn Dent Sci Rev ; 54(2): 88-103, 2018 May.
Artículo en Inglés | MEDLINE | ID: mdl-29755619

RESUMEN

Human cancer tissues are heterogeneous in nature and become differentiated during expansion of cancer stem cells (CSCs). CSCs initiate tumorigenesis, and are involved in tumor recurrence and metastasis. Furthermore, data show that CSCs are highly resistant to anticancer drugs. Cetuximab, a specific anti-epidermal growth factor receptor (EGFR) monoclonal antibody, is used in cancer treatment. Although development of resistance to cetuximab is well recognized, the underlying mechanisms remain unclear. Lapatinib, a dual inhibitor of epidermal growth factor receptor (EGFR)/ErbB2, has antiproliferative effects and is used to treat patients with ErbB2-positive metastatic breast cancer. In this review, cetuximab and lapatinib-resistant oral squamous cell carcinoma (OSCC) cells proliferation and migration signal transduction passway is discussed by introducing our research.

4.
Nagoya J Med Sci ; 80(1): 99-107, 2018 02.
Artículo en Inglés | MEDLINE | ID: mdl-29581619

RESUMEN

The number of patients with diabetes is increasing in Japan. Recently, Social capital (SC) has received increasing attention as a factor influencing health conditions. In the US, the relation between SC and diabetes control has been reported, but little attention has been paid to this connection in Japan. Three SC questionnaires, entitled "trust in people in a community," "social support," and "social relationships," were constructed. The subjects were adult patients with type 2 diabetes. Information on diabetic conditions, such as HbA1c, self-attainment of diet (SAD) and exercise (SAE), and complications were collected. The reliability coefficients for the SC questionnaire and factor analysis of SC were conducted. Multiple and logistic regressions were used to identify the influence of SC on diabetes control. Sixty-five patients participated in this study. The questionnaires "social support" and "social relationships" were adopted to measure Cronbach alpha coefficient. Factor analysis extracted the factors "hope to be helped (HH)," "participation in favorite events (PFE)," "sense of belonging (SB)," and "social movement (SM)." HbA1c was positively correlated with HH (P < 0.05). SAD and SAE were negatively correlated with HH (P < 0.05). SAE was positively correlated with PFE (P < 0.05). PFE reduced complication risks (P < 0.05). HH includes amae, which negatively affected self-efficacy that correlates with diabetes control. Therefore, higher HH might cause higher levels of HbA1c. PFE reduces distress and contributes to glucose control. Reduced distress through PFE might prevent complications. HH and PFE were identified as SC that influences diabetes control.

5.
Am J Hosp Palliat Care ; 35(5): 749-753, 2018 May.
Artículo en Inglés | MEDLINE | ID: mdl-29145731

RESUMEN

BACKGROUND: Although it is recommended that all terminally ill patients receive advance care planning (ACP), this is occasionally challenging because of the difficulty in predicting survival. There are some indexes for predicting survival, but few are accurate, especially at the terminal stages of illness. METHODS: Twenty-two patients at the terminal stages of cancer were retrospectively analyzed. We assessed their physical activity and condition using activities of daily living (ADL) scores for 1 month before the death. The ADL scores included 7 items: walking, bathing, grooming, dressing, eating, transferring, and toileting. RESULTS: Survival time after the first decline of physical activity was calculated (median: 13 days, 95% confidence interval [95% CI]: 5.6-20.4 days). Survival time after the second (median: 5 days, 95% CI: 0-10.9 days), third (median: 5 days, 95% CI: 0-13.4 days), and fourth (median time: 1 day, 95% CI: not applicable due to small size) decline of physical activity was also calculated. CONCLUSION: Change in physical activity seems helpful for estimating survival time, especially at the end of life, and this index could be useful for coordinating final ACP.


Asunto(s)
Actividades Cotidianas , Muerte , Ejercicio , Análisis de Supervivencia , Enfermo Terminal/estadística & datos numéricos , Anciano , Estudios de Cohortes , Femenino , Humanos , Masculino , Persona de Mediana Edad , Monitoreo Ambulatorio , Estudios Retrospectivos , Factores de Tiempo
6.
Yakugaku Zasshi ; 137(6): 733-744, 2017.
Artículo en Japonés | MEDLINE | ID: mdl-28566579

RESUMEN

Collaboration with multiple healthcare professionals is important to provide safer and higher quality care. Interprofessional education (IPE) promotes the practice of team-based care. The establishment of Tsurumai-Meijo IPE, including interprofessional education and practice (IPEP) and video-teaching materials, was conducted in collaboration with school of medicine/nursing in Nagoya University and Fujita Health University, because Meijo University does not have its own clinical settings and faculties except for pharmacy. In the established Tsurumai-Meijo IPE, pharmacy, medicine, and nursing students interviewed simulated patients (SP) together or separately and practiced team-based care through Tsurumai-Meijo IPEP. Students could learn in advance and on their own about each professional's knowledge related to patient care by using video-teaching materials from the Meijo IPE homepage. Using a questionnaire survey at the end of program, this study was examined whether Tsurumai-Meijo IPEP, and video-teaching materials were useful for understanding importance of team-based care. More than 83% of students indicated that Tsurumai-Meijo IPE is useful on future clinical practice. This suggests that the program and materials are beneficial to the medical student education. In the optional survey of some clinical pharmacists, who had participated in Tsurumai-Meijo IPE before graduation, they utilized it in their work and it facilitated their work related to team-based care. Tsurumai-Meijo IPE collaborating with SP is likely to contribute to provide high quality and safe team-based care by taking advantage of specialized professional ability of healthcare professionals.


Asunto(s)
Educación Médica/métodos , Educación en Enfermería/métodos , Educación en Farmacia/métodos , Colaboración Intersectorial , Simulación de Paciente , Competencia Clínica , Femenino , Humanos , Masculino , Grupo de Atención al Paciente , Calidad de la Atención de Salud , Encuestas y Cuestionarios , Materiales de Enseñanza , Grabación de Cinta de Video
7.
Oncol Rep ; 37(6): 3674-3680, 2017 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-28440510

RESUMEN

The activation of receptor tyrosine kinases (RTKs) results in cellular effects including cell proliferation, survival, migration and invasion; RTKs also play an important role in tumourigenesis. It has been reported that EGFR signalling controls the migration of oral squamous cell carcinoma (OSCC) SAS and HSC3 cells but not of HSC4 cells, although the proliferation of HSC4 cells is regulated by EGF/EGFR. In the present study, we investigated the roles of EGFR and the c-Met signalling pathway in cell migration via filopodia and lamellipodia formation, which may be prerequisites for migration. To explore the role of c-Met in cell migration, we inhibited c-Met RTK activity using the c-Met inhibitor SU11274 and activated c-Met using hepatocyte growth factor (HGF) in three OSCC cell lines HSC4, SAS and Ca9-22 and investigated migration potency using a wound healing assay. We showed that inhibition of c-Met significantly suppressed, and activation of c-Met significantly promoted, the migration of OSCC cells. Additionally, the migration of SAS and Ca9-22 cells was inhibited by the EGFR inhibitors AG1478 and cetuximab and promoted by EGF treatment. Moreover, migration potency was correlated with lamellipodia formation. Furthermore, western blot analyses demonstrated that SU11274 decreased and HGF increased lamellipodin protein levels as well as phosphorylated c-Met levels. Collectively, we demonstrated that c-Met signalling induced lamellipodia formation by upregulating lamellipodin, thereby promoting the migration of OSCC cells.


Asunto(s)
Carcinoma de Células Escamosas/tratamiento farmacológico , Receptores ErbB/genética , Neoplasias de la Boca/tratamiento farmacológico , Proteínas Proto-Oncogénicas c-met/genética , Carcinoma de Células Escamosas/genética , Carcinoma de Células Escamosas/patología , Línea Celular Tumoral , Movimiento Celular/efectos de los fármacos , Movimiento Celular/genética , Proliferación Celular/efectos de los fármacos , Cetuximab/administración & dosificación , Factor de Crecimiento Epidérmico/genética , Factor de Crecimiento Epidérmico/metabolismo , Receptores ErbB/antagonistas & inhibidores , Factor de Crecimiento de Hepatocito/genética , Factor de Crecimiento de Hepatocito/metabolismo , Humanos , Indoles/administración & dosificación , Neoplasias de la Boca/genética , Neoplasias de la Boca/patología , Fosfatidilinositol 3-Quinasas/genética , Piperazinas/administración & dosificación , Proteínas Proto-Oncogénicas c-akt/genética , Proteínas Proto-Oncogénicas c-met/antagonistas & inhibidores , Seudópodos/efectos de los fármacos , Seudópodos/genética , Quinazolinas/administración & dosificación , Transducción de Señal/efectos de los fármacos , Sulfonamidas/administración & dosificación , Tirfostinos/administración & dosificación
8.
Oncol Lett ; 13(2): 930-936, 2017 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-28356980

RESUMEN

Cell migration potency is essential in cancer metastasis and is often regulated by extracellular stimuli. Oral squamous cell carcinoma cell lines include those that are sensitive, as well as resistant, to the effects of the epidermal growth factor receptor (EGFR) inhibitor cetuximab on cell migration. In the present study, the molecular differences in the EGFR response to cell migration between the SAS cetuximab-sensitive and HSC4 cetuximab-resistant cell lines was examined. Treatment with the EGFR inhibitors AG1478 and cetuximab reduced the migration potency of SAS cells, but not HSC4 cells. The migration of the two cell lines was inhibited under serum-free culture conditions, and the addition of EGF to the serum-free medium promoted the migration of SAS cells, but not HSC4 cells. In addition, SAS cell migration was reduced by the mitogen-activated protein kinase kinase and protein kinase B (Akt) inhibitors PD98059 and MK2206, whereas HSC4 cell migration was only inhibited by MK2206. EGF induced an increase in extracellular signal-regulated kinase phosphorylation levels in HSC4 cells, and stimulated Akt phosphorylation levels in SAS cells. Furthermore, the staining of actin filaments with phalloidin was significantly increased by the inhibition of EGFR in SAS cells, but was not observed as altered in HSC4 cells. Conversely, the addition of EGF to the culture medium decreased the accumulation of actin filaments in SAS cells. The results suggest that the EGF-EGFR signaling pathway has an important role in SAS cell migration via the modulation of actin dynamics, and that HSC4 cell migration is regulated by a serum component other than EGFR.

9.
Oncol Rep ; 36(5): 3058-3064, 2016 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-27633099

RESUMEN

Lapatinib, a dual inhibitor of epidermal growth factor receptor (EGFR)/ErbB2, has antiproliferative effects and is used to treat patients with ErbB2-positive metastatic breast cancer. In the present study, we examined the effects of lapatinib on growth of oral and prostate cancer cells. Oral squamous cell carcinoma (OSCC) cell lines HSC3, HSC4 and Ca9-22 were sensitive to the antiproliferative effects of lapatinib in anchorage-dependent culture, but the OSCC cell lines KB and SAS and the prostate cancer cell line DU145 were resistant to lapatinib. Phosphorylation levels of EGFR in all cell lines decreased during lapatinib treatment in anchorage­dependent culture. Furthermore, the phosphorylation levels of ErbB2, ErbB3 and Akt and the protein levels of cyclin D1 were decreased by lapatinib treatment of HSC3, HSC4 and Ca9-22 cells. ErbB3 was not expressed and cyclin D1 protein levels were not altered by lapatinib treatment in KB, DU145 and SAS cells. The phosphorylation of ErbB2 and AKT was not affected by lapatinib in SAS cells and was not detected in KB and DU145 cells. Lapatinib-resistant cell lines exhibited sphere-forming ability, and SAS cells developed sensitivity to lapatinib during sphere formation. The phosphorylation levels of ErbB2 and AKT and protein levels of cyclin D2 increased during sphere formation of SAS cells and decreased with lapatinib treatment. In addition, sphere formation of SAS cells was inhibited by the AKT inhibitor MK2206. AKT phosphorylation and cyclin D2 levels in SAS spheres were decreased by MK2206 treatment. SAS cells expressed E-cadherin, but not vimentin and KB cells expressed vimentin, but not E-cadherin. DU145 cells expressed vimentin and E-cadherin. These results suggested that phosphorylation of EGFR and ErbB2 by cell detachment from the substratum induces the AKT pathway/cyclin D2-dependent sphere growth in SAS epithelial cancer stem-like cells, thereby rendering SAS spheres sensitive to lapatinib treatment.


Asunto(s)
Carcinoma de Células Escamosas/tratamiento farmacológico , Ciclina D1/biosíntesis , Ciclina D2/biosíntesis , Neoplasias de la Boca/tratamiento farmacológico , Neoplasias de la Próstata/tratamiento farmacológico , Proteínas Proto-Oncogénicas c-akt/biosíntesis , Receptor ErbB-2/biosíntesis , Receptor ErbB-3/biosíntesis , Cadherinas/biosíntesis , Carcinoma de Células Escamosas/genética , Carcinoma de Células Escamosas/patología , Línea Celular Tumoral , Ciclina D1/genética , Ciclina D2/genética , Resistencia a Antineoplásicos/efectos de los fármacos , Receptores ErbB/biosíntesis , Receptores ErbB/genética , Femenino , Regulación Neoplásica de la Expresión Génica , Humanos , Lapatinib , Masculino , Neoplasias de la Boca/genética , Neoplasias de la Boca/patología , Fosforilación , Neoplasias de la Próstata/genética , Neoplasias de la Próstata/patología , Proteínas Proto-Oncogénicas c-akt/genética , Quinazolinas/administración & dosificación , Receptor ErbB-2/genética , Receptor ErbB-3/genética
10.
Oncol Rep ; 36(1): 514-20, 2016 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-27121913

RESUMEN

Early detection of precancerous and early cancerous lesions could greatly reduce both the mortality and morbidity of oral cancer. The objective of this study was to analyze a fluorescence visualization (FV) system for the detection of precancerous and early cancerous lesions in rat tongue carcinogenesis and human oral cancerous lesions using for the first time a 4NQO rat model and human tissue. Based on the results from the rat tongue carcinogenesis model, under direct FV, the normal oral mucosa emitted various shades of pale green autofluorescence. In the precancerous and early cancerous cases, the lesion appeared as an irregular dark area. Histological examination of the lesions showed that the VELscope system had a sensitivity of 95% and specificity of 100% in discriminating normal mucosa from dysplasia/carcinoma in situ (CIS) or invasive carcinoma. The proliferating cell nuclear antigen (PCNA) protein level was gradually increased with progression of carcinogenic transformation. Furthermore, the results of PCNA and FV loss (FVL) were correlated. Next, results from 17 patients were also presented. Histological examination of the lesions showed that the VELscope system had a sensitivity of 95% and specificity of 100% in discriminating normal mucosa from severe dysplasia/CIS or invasive carcinoma. There were no normal epithelium cells in any of the FVL regions. Furthermore, to clarify the usefulness of FV compared to vital staining with iodine, we investigated the surgical margins of early oral squamous cell carcinoma (OSCC) tissues and compared the FVL and iodine unstained area (IU). The percentage of various types of dysplasia were almost equal when comparing the FVL and IU. These results suggest that this direct FV device has the potential for simple, cost-effective screening, detection and margin determination of oral precancerous and early cancerous lesions.


Asunto(s)
Neoplasias de la Boca/diagnóstico , Lesiones Precancerosas/diagnóstico , Animales , Carcinogénesis/patología , Carcinoma in Situ/diagnóstico , Carcinoma in Situ/patología , Carcinoma de Células Escamosas/diagnóstico , Carcinoma de Células Escamosas/patología , Epitelio/patología , Fluorescencia , Humanos , Masculino , Mucosa Bucal/patología , Neoplasias de la Boca/patología , Lesiones Precancerosas/patología , Ratas , Ratas Sprague-Dawley , Sensibilidad y Especificidad
11.
Heart Vessels ; 31(6): 990-5, 2016 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-25794983

RESUMEN

Gadolinium contrast agents used for late gadolinium enhancement (LGE) distribute in the extracellular space. Global diffuse myocardial LGE pronounced in the subendocardial layers is common in cardiac amyloidosis. However, the pathophysiological basis of these findings has not been sufficiently explained. A 64-year-old man was admitted to our hospital with leg edema and nocturnal dyspnea. Bence Jones protein was positive in the urine, and an endomyocardial and skin biopsy showed light-chain (AL) amyloidosis. He died of ventricular fibrillation 3 months later. 9 days before death, the patient was examined by cardiac magnetic resonance (CMR) imaging on a 3-T system. We acquired LGE data at 2, 5, 10, and 20 min after the injection of gadolinium contrast agents, with a fixed inversion time of 350 ms. Myocardial LGE developed sequentially. The myocardium was diffusely enhanced at 2 min, except for the subendocardium, but LGE had extended to almost the entire left ventricle at 5 min and predominantly localized to the subendocardial region at 10 and 20 min. An autopsy revealed massive and diffused amyloid deposits in perimyocytes throughout the myocardium. Old and recent ischemic findings, such as replacement fibrosis and coagulative myocyte necrosis, were evident in the subendocardium. In the intramural coronary arteries, mild amyloid deposits were present within the subepicardial to the mid layer of the left ventricle, but no stenotic lesions were evident. However, capillaries were obstructed by amyloid deposits in the subendocardium. In conclusion, the late phase of dynamic LGE (at 10 and 20 min) visualized in the subendocardium corresponded to the interstitial amyloid deposition and subendocardial fibrosis caused by ischemia in our patient.


Asunto(s)
Amiloide/análisis , Amiloidosis/diagnóstico por imagen , Cardiomiopatías/diagnóstico por imagen , Medios de Contraste/administración & dosificación , Enfermedad de la Arteria Coronaria/diagnóstico por imagen , Vasos Coronarios/diagnóstico por imagen , Gadolinio DTPA/administración & dosificación , Imagen por Resonancia Magnética , Imagen de Perfusión Miocárdica/métodos , Miocardio , Amiloidosis/metabolismo , Amiloidosis/patología , Amiloidosis/fisiopatología , Autopsia , Cardiomiopatías/metabolismo , Cardiomiopatías/patología , Cardiomiopatías/fisiopatología , Enfermedad de la Arteria Coronaria/metabolismo , Enfermedad de la Arteria Coronaria/patología , Enfermedad de la Arteria Coronaria/fisiopatología , Circulación Coronaria , Vasos Coronarios/química , Vasos Coronarios/patología , Vasos Coronarios/fisiopatología , Resultado Fatal , Fibrosis , Humanos , Masculino , Persona de Mediana Edad , Miocardio/química , Miocardio/patología , Valor Predictivo de las Pruebas
12.
Int J Oncol ; 47(6): 2165-72, 2015 Dec.
Artículo en Inglés | MEDLINE | ID: mdl-26497980

RESUMEN

We have previously shown that growth of the oral squamous cell carcinoma cell line SAS, is resistant to cetuximab in monolayer culture conditions, even though epidermal growth factor receptor (EGFR) was phosphorylated, but the growth of SAS aggregates was sensitive to cetuximab. In the present study, we demonstrate differences in the EGFR signaling pathways utilized by SAS cells in monolayer and suspension cultures at the molecular level. Cetuximab treatment of SAS cells in monolayer cultures inhibits the phosphorylation of EGFR and ERK, and reduces the cell migratory potency, but not cell proliferation. AG1478 treatment reduces the phosphorylation of EGFR, ERK and AKT, and affects cell growth in monolayer cultures. The phosphorylation levels of EGFR and AKT are significantly higher in SAS cell aggregates compared to monolayer cultures. Treatment with cetuximab and AG1478 reduces the growth of SAS aggregates and eliminates the phosphorylation of EGFR and AKT. Furthermore, proliferation of SAS aggregates is also inhibited by LY294002 and MK2206, which are inhibitors of PI3K and AKT, respectively. In addition, treatment with the lipid raft disruptor filipin III reduced the phosphorylation levels of EGFR and Akt in SAS aggregates, but not in SAS monolayer culture. These results suggest the possibility that ligands in the serum stimulate the phosphorylation of EGFR localized in lipid rafts leading to PI3K-AKT activation, which results in the growth of SAS aggregates, therefore resulting in the sensitivity of SAS aggregates to cetuximab.


Asunto(s)
Antineoplásicos/farmacología , Carcinoma de Células Escamosas/patología , Técnicas de Cultivo de Célula/métodos , Cetuximab/farmacología , Resistencia a Antineoplásicos/fisiología , Neoplasias de la Boca/patología , Western Blotting , Carcinoma de Células Escamosas/metabolismo , Línea Celular Tumoral , Movimiento Celular/efectos de los fármacos , Movimiento Celular/fisiología , Proliferación Celular/efectos de los fármacos , Proliferación Celular/fisiología , Resistencia a Antineoplásicos/efectos de los fármacos , Receptores ErbB/metabolismo , Técnica del Anticuerpo Fluorescente , Humanos , Neoplasias de la Boca/metabolismo , Fosforilación , Proteínas Proto-Oncogénicas c-akt/metabolismo , Transducción de Señal/efectos de los fármacos , Transducción de Señal/fisiología
13.
Nat Commun ; 6: 7527, 2015 Jul 06.
Artículo en Inglés | MEDLINE | ID: mdl-26146385

RESUMEN

Damaged mitochondria are removed by mitophagy. Although Atg32 is essential for mitophagy in yeast, no Atg32 homologue has been identified in mammalian cells. Here, we show that Bcl-2-like protein 13 (Bcl2-L-13) induces mitochondrial fragmentation and mitophagy in mammalian cells. First, we hypothesized that unidentified mammalian mitophagy receptors would share molecular features of Atg32. By screening the public protein database for Atg32 homologues, we identify Bcl2-L-13. Bcl2-L-13 binds to LC3 through the WXXI motif and induces mitochondrial fragmentation and mitophagy in HEK293 cells. In Bcl2-L-13, the BH domains are important for the fragmentation, while the WXXI motif facilitates mitophagy. Bcl2-L-13 induces mitochondrial fragmentation in the absence of Drp1, while it induces mitophagy in Parkin-deficient cells. Knockdown of Bcl2-L-13 attenuates mitochondrial damage-induced fragmentation and mitophagy. Bcl2-L-13 induces mitophagy in Atg32-deficient yeast cells. Induction and/or phosphorylation of Bcl2-L-13 may regulate its activity. Our findings offer insights into mitochondrial quality control in mammalian cells.


Asunto(s)
Mitocondrias/fisiología , Degradación Mitocondrial/fisiología , Proteínas Proto-Oncogénicas c-bcl-2/metabolismo , GTP Fosfohidrolasas/genética , GTP Fosfohidrolasas/metabolismo , Regulación de la Expresión Génica/fisiología , Células HEK293 , Células HeLa , Humanos , Proteínas Asociadas a Microtúbulos/genética , Proteínas Asociadas a Microtúbulos/metabolismo , Proteínas Mitocondriales/genética , Proteínas Mitocondriales/metabolismo , Proteínas Proto-Oncogénicas c-bcl-2/genética
15.
Oncol Lett ; 9(2): 833-836, 2015 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-25621058

RESUMEN

Infiltrating angiolipoma (IAL) is a rare lesion and is a clinicopathological variant of angiolipoma. IAL occurs most commonly in the trunk and extremities, it is rarely found in the head and neck regions and extremely rare in the oral cavity. This study presents the case of a 74-year-old female with IAL of the lower lip. To the best of our knowledge, this is the first case of IAL arising in the lower lip to be reported. Microscopically, IAL was unencapsulated and mature lipocytes were separated by a branching network of proliferating small vessels that infiltrated the adjacent tissues. Therefore, complete excision was difficult to perform. Magnetic resonance imaging has been reported to be valuable in determining the extent of the tumor and asserting a preoperative diagnosis. According to previous studies, the recurrence rate of IAL following surgical extirpation is 35-50%. Furthermore, the levels of mRNA expression of the vascular endothelial growth factor (VEGF) family members in the tumor were investigated. VEGF-A and -B expression were detected, however, VEGF-C and -D were expressed at extremely low levels. Excisional biopsy was performed under local anesthesia. During four years of follow-up, no evidence of tumor recurrence had been identified. An operating microscope may be utilized for the total removal of an IAL to minimize damage to normal tissues. This report indicates that mast cell-derived VEGF may be responsible for the enhanced vascularity in the tumor. We would therefore consider careful extirpation with no wide safety margin to be the procedure of choice, except when the tumor invades irregularly into the muscles.

16.
Oncol Lett ; 7(5): 1439-1442, 2014 May.
Artículo en Inglés | MEDLINE | ID: mdl-24765152

RESUMEN

Epidermal growth factor (EGF) is present at high concentrations in human saliva and modulates the growth and differentiation of various cancer cells. To elucidate the molecular mechanisms by which EGF affects oral cancer proliferation and invasion, the current study analyzed the Matrigel invasion activity of cultured oral cancer cell lines. Cell proliferation under the influence of EGF was subjected to Matrigel invasion assays, and cell proliferation in the absence of EGF was used as control. Northern blot analyses quantified the invasiveness and tumorigenicity. Chloramphenicol acetyltransferase assay determined the EGF stimulation of matrix metalloproteinase (MMP) 1 expression. EGF increased the number of cells penetrating the Matrigel membrane. Northern blot analysis revealed that MMP1 and cytokeratin 19 expression correlate with EGF. In addition, the morphology of HSC-3 and SAS cells changed following the addition of EGF to the culture medium. A transient transfection assay revealed that EGF increases the promoter activities of MMP1 in HSC-3 cells. These observations suggested that EGF increases the invasive activity of oral cancer cells, partly by increasing MMP1, and morphological changes may be induced by altering the composition of cytoskeletal proteins.

17.
Fam Pract ; 31(1): 118-26, 2014 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-24115011

RESUMEN

BACKGROUND: Empathy is an important attribute in medicine, influencing both the process and outcome of consultations. However, there are no validated tools available in Japan to gather patient feedback on physicians' empathy. The Consultation and Relational Empathy (CARE) Measure developed in the UK is widely used internationally. OBJECTIVES: To investigate the psychometric properties of a Japanese version of the CARE Measure. METHOD: Following two cycles of translation and back translation, the Japanese CARE Measure was completed by 317 patients in a primary medical care clinic in Japan. Tests of internal reliability and validity included Cronbach's alpha, item-total correlations and factor analysis. Predicted associations between CARE Measure score and other variables were assessed by Spearman's rho. RESULTS: Low numbers of missing values (8.2-9.8%) and 'not applicable' responses (0-1.3%) suggested high acceptability and face validity of the Japanese CARE Measure. Internal reliability was high (Cronbach's alpha 0.984) and was reduced by the removal of any of 10 items. High corrected item-total correlations (0.897-0.946) suggested homogeneity. Factor analysis showed a single solution with high item loadings (0.917-0.957). Construct validity was supported by a significant relationship (Spearman's rho 0.74, P < 0.001) with overall satisfaction with the consultation. CONCLUSION: The Japanese CARE Measure appears to be valid and reliable in a primary medical care setting. Further work is required to determine its ability to discriminate between doctors.


Asunto(s)
Competencia Clínica , Empatía , Relaciones Médico-Paciente , Atención Primaria de Salud , Adulto , Anciano , Atención Ambulatoria , Análisis Factorial , Femenino , Medicina General , Humanos , Japón , Lenguaje , Masculino , Persona de Mediana Edad , Psicometría/instrumentación , Calidad de la Atención de Salud , Reproducibilidad de los Resultados , Encuestas y Cuestionarios
18.
Biochem Biophys Res Commun ; 441(4): 787-92, 2013 Nov 29.
Artículo en Inglés | MEDLINE | ID: mdl-24211573

RESUMEN

Cardiac hypertrophy occurs in response to a variety of stresses as a compensatory mechanism to maintain cardiac output and normalize wall stress. Prevention or regression of cardiac hypertrophy can be a major therapeutic target. Although regression of cardiac hypertrophy occurs after control of etiological factors, the molecular mechanisms remain to be clarified. In the present study, we investigated the role of autophagy in regression of cardiac hypertrophy. Wild-type mice showed cardiac hypertrophy after continuous infusion of angiotensin II for 14 days using osmotic minipumps, and regression of cardiac hypertrophy was observed 7 days after removal of the minipumps. Autophagy was induced during regression of cardiac hypertrophy, as evidenced by an increase in microtubule-associated protein 1 light chain 3 (LC3)-II protein level. Then, we subjected cardiac-specific Atg5-deficient (CKO) and control mice (CTL) to angiotensin II infusion for 14 days. CKO and CTL developed cardiac hypertrophy to a similar degree without contractile dysfunction. Seven days after removal of the minipumps, CKO showed significantly less regression of cardiac hypertrophy compared with CTL. Regression of pressure overload-induced cardiac hypertrophy after unloading was also attenuated in CKO. These results suggest that autophagy is necessary for regression of cardiac hypertrophy during unloading of neurohumoral and hemodynamic stress.


Asunto(s)
Autofagia , Cardiomegalia/patología , Cardiomegalia/fisiopatología , Ventrículos Cardíacos/fisiopatología , Angiotensina II/farmacología , Animales , Proteína 5 Relacionada con la Autofagia , Cardiomegalia/inducido químicamente , Modelos Animales de Enfermedad , Ratones , Ratones Mutantes , Proteínas Asociadas a Microtúbulos/genética , Proteínas Asociadas a Microtúbulos/metabolismo
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