RESUMEN
BACKGROUND: This study investigated the causes of dental implant removal due to complications, and examined whether patients who had dental implant removal desired re-implant prosthesis treatments. MATERIAL AND METHODS: A retrospective case-control study was conducted on patients who had their dental implants removed. We investigated whether the removed dental implant was replaced with other implant prostheses. Age, sex, diabetes, smoking, implant site distribution, reason for implant removal, and blade and root-form implants were categorized as predictive variables. The outcome variable was desire for re-implantation or use of other prosthetic methods after implant removal. A logistic regression model was created to identify patient factors that could predict the re-implantation of dental prostheses after implant removal. RESULTS: A total of 215 dental implants were removed from 143 patients. The most common reason for implant removal was peri-implantitis that was identified in 165 implants. After implant removal, re-implantation was performed in 98 implants (45.6%). Bivariate analyses showed that age, diabetes, implant type, and reason for implant removal were associated with the desire for re-implanted prostheses. The multiple regression model revealed that age, implant type, and reason for implant removal were associated with an increased desire for re-implant prostheses after implant removal. CONCLUSIONS: Re-implantation of prostheses after the removal of dental implants was desired by patients who were younger, had implants placed in the root form, and had implants removed due to prosthetic-related complications.
Asunto(s)
Implantes Dentales , Estudios de Casos y Controles , Implantación Dental Endoósea , Diseño de Prótesis Dental , Prótesis Dental de Soporte Implantado , Fracaso de la Restauración Dental , Estudios de Seguimiento , Humanos , Estudios RetrospectivosRESUMEN
Mutations in ASXL1 are frequent in patients with myelodysplastic syndrome (MDS) and are associated with adverse survival, yet the molecular pathogenesis of ASXL1 mutations (ASXL1-MT) is not fully understood. Recently, it has been found that deletion of Asxl1 or expression of C-terminal-truncating ASXL1-MTs inhibit myeloid differentiation and induce MDS-like disease in mice. Here, we find that SET-binding protein 1 (SETBP1) mutations (SETBP1-MT) are enriched among ASXL1-mutated MDS patients and associated with increased incidence of leukemic transformation, as well as shorter survival, suggesting that SETBP1-MT play a critical role in leukemic transformation of MDS. We identify that SETBP1-MT inhibit ubiquitination and subsequent degradation of SETBP1, resulting in increased expression. Expression of SETBP1-MT, in turn, inhibited protein phosphatase 2A activity, leading to Akt activation and enhanced expression of posterior Hoxa genes in ASXL1-mutant cells. Biologically, SETBP1-MT augmented ASXL1-MT-induced differentiation block, inhibited apoptosis and enhanced myeloid colony output. SETBP1-MT collaborated with ASXL1-MT in inducing acute myeloid leukemia in vivo. The combination of ASXL1-MT and SETBP1-MT activated a stem cell signature and repressed the tumor growth factor-ß signaling pathway, in contrast to the ASXL1-MT-induced MDS model. These data reveal that SETBP1-MT are critical drivers of ASXL1-mutated MDS and identify several deregulated pathways as potential therapeutic targets in high-risk MDS.
Asunto(s)
Proteínas Portadoras/genética , Transformación Celular Neoplásica/genética , Regulación Leucémica de la Expresión Génica , Leucemia Mieloide Aguda/genética , Síndromes Mielodisplásicos/genética , Proteínas Nucleares/genética , Proteínas Represoras/genética , Adulto , Animales , Apoptosis , Proteínas Portadoras/metabolismo , Diferenciación Celular , Transformación Celular Neoplásica/metabolismo , Transformación Celular Neoplásica/patología , Células HEK293 , Células HL-60 , Proteínas de Homeodominio/genética , Proteínas de Homeodominio/metabolismo , Humanos , Leucemia Mieloide Aguda/metabolismo , Leucemia Mieloide Aguda/mortalidad , Leucemia Mieloide Aguda/patología , Ratones , Ratones Endogámicos C57BL , Mutación , Síndromes Mielodisplásicos/metabolismo , Síndromes Mielodisplásicos/mortalidad , Síndromes Mielodisplásicos/patología , Proteínas Nucleares/metabolismo , Proteína Fosfatasa 2/genética , Proteína Fosfatasa 2/metabolismo , Proteolisis , Proteínas Proto-Oncogénicas c-akt/genética , Proteínas Proto-Oncogénicas c-akt/metabolismo , Proteínas Represoras/metabolismo , Transducción de Señal , Análisis de Supervivencia , Factor de Crecimiento Transformador beta/genética , Factor de Crecimiento Transformador beta/metabolismo , UbiquitinaciónRESUMEN
Osteoprotegerin (OPG) is a recently identified member of the tumor necrosis factor (TNF) receptor superfamily that regulates bone mass through an inhibitory action on osteoclast differentiation and function. To determine its potential roles of OPG in pathological changes in bone metabolism caused by estrogen deficiency, we investigated effects of estrogen on OPG expression by a mouse stromal cell line, ST-2, in vitro. Treatment of ST-2 cells with 17beta-E(2) resulted in up-regulation of OPG expression at both the messenger RNA and protein levels. The effect was time and dose dependent and steroid specific. The stimulatory action of 17beta-E(2) on OPG expression appeared to be mediated by the estrogen receptor-alpha (ERalpha) subtype because stable overexpression of ERalpha, but not of ERbeta, enhanced the OPG induction by 17beta-E(2). Moreover, estrogen withdrawal after 5-day pretreatment, mimicking the event occurring in vivo at menopause, dramatically diminished the expression of OPG. These findings suggest that down-regulation of OPG after estrogen withdrawal contributes to the enhanced osteoclastic bone resorption and bone loss after menopause by enhancing RANK ligand-RANK system that lies downstream of a large number of bone-resorbing cytokines.
Asunto(s)
Estradiol/farmacología , Expresión Génica/efectos de los fármacos , Glicoproteínas/genética , Receptores Citoplasmáticos y Nucleares/genética , Receptores de Estrógenos/fisiología , Células del Estroma/metabolismo , Animales , Línea Celular , Relación Dosis-Respuesta a Droga , Estradiol/administración & dosificación , Receptor alfa de Estrógeno , Glicoproteínas/análisis , Humanos , Cinética , Ratones , Osteoprotegerina , ARN Mensajero/análisis , Receptores Citoplasmáticos y Nucleares/análisis , Receptores de Estrógenos/efectos de los fármacos , Receptores del Factor de Necrosis TumoralRESUMEN
The aims of this study were to determine 1) which cells are involved in stress-induced acute gastric mucosal lesion and 2) what kinds of molecular alterations are induced by stress, using immediate-early genes (IEG) as tools for detection of cellular activation. Male Wistar rats were exposed to acute water immersion-restraint stress. Protein and mRNA for IEG were detected by immunohistochemistry and in situ hybridization, respectively. This stress induced the expression of c-fos and nerve growth factor-induced gene (NGFI-A) mRNA in gastric epithelial cells, the smooth muscle layer of small blood vessels, and the stomach wall. Stress upregulated the mRNA levels of these IEG in the duodenal epithelial cells and induced de novo expression of IEG in the smooth muscle layer of small blood vessels and the duodenal wall. These findings indicate that these cells are activated in response to stress. Expression of these IEG and/or transcriptional factors may reflect an initiation of mechanisms for repairing the lesions induced by stress as well as an adaptation to the stress.
Asunto(s)
Duodeno/metabolismo , Mucosa Gástrica/metabolismo , Regulación de la Expresión Génica , Genes Inmediatos-Precoces , Genes fos , Proteínas Inmediatas-Precoces , Mucosa Intestinal/metabolismo , Músculo Liso/metabolismo , Estrés Psicológico/metabolismo , Animales , Proteínas de Unión al ADN/biosíntesis , Proteínas de Unión al ADN/genética , Duodeno/irrigación sanguínea , Proteína 1 de la Respuesta de Crecimiento Precoz , Genes jun , Inmersión , Inmunohistoquímica , Hibridación in Situ , Masculino , Músculo Liso/irrigación sanguínea , Músculo Liso Vascular/metabolismo , Biosíntesis de Proteínas , Proteínas Proto-Oncogénicas c-fos/biosíntesis , Proteínas Proto-Oncogénicas c-fos/genética , Proteínas Proto-Oncogénicas c-jun/biosíntesis , Proteínas Proto-Oncogénicas c-jun/genética , ARN Mensajero/biosíntesis , Ratas , Ratas Wistar , Restricción Física , Estómago/irrigación sanguínea , Factores de Transcripción/biosíntesis , Factores de Transcripción/genética , Transcripción Genética , Dedos de ZincRESUMEN
We investigated the effects of peripherally administered 5-HT on the secondary neurons in the spinal cord of rats using Fos-like immunoreactivity (FLI) as a marker of neuronal activation. The intradermal administration of 5-HT (30, 60 microg) induced a large number of FLI neurons in the ipsilateral dorsal horn. In animals given 5-HT2A receptor agonists (DOI: 0.28 to 2.8 micromol/kg, alpha-methyl 5-HT: 0.28 to 2.8 micromol/kg) intradermally, immunoreactive neurons were evoked in the same manner as those given 5-HT. Other agonists, including 5-HT3 receptor agonists (m-CPG: 16 to 32 micromol/kg, 2-methyl 5-HT: 0.0028 to 2.8 micromol/kg), did not induce FLI neurons at any dose examined. Furthermore, 5-HT2A receptor antagonist (ketanserin: 1 mg/kg, i.p.) suppressed the expression of FLI in the dorsal horn caused by peripheral 5-HT, but 5-HT3 receptor antagonist (tropisetron: 1 mg/kg, i.p.) did not. These findings suggest that the 5-HT-induced nociceptive response is mediated by 5-HT2A receptors in the periphery.