RESUMEN
This paper presents some advances in condition monitoring for rotary machines (particularly for a lathe headstock gearbox) running idle with a constant speed, based on the behaviour of a driving three-phase AC asynchronous induction motor used as a sensor of the mechanical power via the absorbed electrical power. The majority of the variable phenomena involved in this condition monitoring are periodical (machines having rotary parts) and should be mechanically supplied through a variable electrical power absorbed by a motor with periodical components (having frequencies equal to the rotational frequency of the machine parts). The paper proposes some signal processing and analysis methods for the variable part of the absorbed electrical power (or its constituents: active and instantaneous power, instantaneous current, power factor, etc.) in order to achieve a description of these periodical constituents, each one often described as a sum of sinusoidal components with a fundamental and some harmonics. In testing these methods, the paper confirms the hypothesis that the evolution of the electrical power (instantaneous and active) has a predominantly deterministic character. Two main signal analysis methods were used, with good, comparable results: the fast Fourier transform of short and long signal sequences (for the frequency domain) and the curve fitting estimation (in the time domain). The determination of the amplitude, frequency and phase at origin of time for each of these components helps to describe the condition (normal or abnormal) of the machine parts. Several achievements confirm the viability of this study: a characterization of a flat driving belt condition and a beating power phenomenon generated by two rotary shafts inside the gearbox. For comparison purposes, the same signal analysis methods were applied to describe the evolution of the vibration signal and the instantaneous angular speed signal at the gearbox output spindle. Many similarities in behaviour among certain mechanical parts (including their electrical power, vibration and instantaneous angular speed) were highlighted.
Asunto(s)
Electricidad , Procesamiento de Señales Asistido por Computador , VibraciónRESUMEN
PURPOSE: Capsular tension rings (CTRs) are commonly used for stabilizing the capsule in lax zonules. Blind and uncontrolled maneuvering of the ring free end may cause intraoperative incidents during CTR insertion. We improved the design of a standard CTR typical injector that eliminates the risks associated with the lack of control during its insertion. METHODS: We present a modification of a typical injector used for insertion of standard CTR as well as the insertion technique. The modification consists of a metal anchoring element attached to the free end of the tube, on which the second eyelet of a standard CTR is fixed. The device was used in the surgical treatment of 50 adult patients with cataract associated with lax zonule. RESULTS: The improved injector led to a reduced injection duration and complexity, and there were no intraoperative incidents or postoperative complications. CONCLUSIONS: The fixation of the second eyelet allows a controlled insertion of the standard CTRs, which facilitates the intraocular implantation technique, reduces surgical complications associated with the blind maneuvering of the free end of the ring inserted by traditional methods, and has a less disruptive action on the integrity of the remaining undamaged zonular fibers in the lax zonules. The accessory attached to the typical injector tube reduces the risk of surgical incidents caused by the uncontrolled progression of the ring's free end inside the capsular bag.
Asunto(s)
Ligamentos , Enfermedades Musculoesqueléticas/patología , Facoemulsificación/métodos , Prótesis e Implantes , Implantación de Prótesis/instrumentación , Adulto , Anciano , Femenino , Humanos , Cápsula del Cristalino/cirugía , Masculino , Persona de Mediana Edad , Complicaciones PosoperatoriasRESUMEN
The functional relevance of brain-derived neurotrophic factor (BDNF) is beginning to be well appreciated not only in mice, but also in humans. Because reduced levels typically correlate with impaired neuronal function, increasing BDNF levels with well-tolerated drugs diffusing into the central nervous system may help in ameliorating functional deficits. With this objective in mind, we used the sphingosine-1 phosphate receptor agonist fingolimod, a drug that crosses the blood-brain barrier. In addition, fingolimod has recently been introduced as the first oral treatment for multiple sclerosis. In cultured neurons, fingolimod increases BDNF levels and counteracts NMDA-induced neuronal death in a BDNF-dependent manner. Ongoing synaptic activity and MAPK signaling is required for fingolimod-induced BDNF increase, a pathway that can also be activated in vivo by systemic fingolimod administration. Mice lacking Mecp2, a gene frequently mutated in Rett syndrome, show decreased levels of BDNF, and fingolimod administration was found to partially rescue these levels as well as the size of the striatum, a volumetric sensor of BDNF signaling in rodents. These changes correlate with increased locomotor activity of the Mecp2-deficient animals, suggesting that fingolimod may improve the functional output of the nervous system, in addition to its well-documented effects on lymphocyte egress from lymph nodes.
Asunto(s)
Factor Neurotrófico Derivado del Encéfalo/metabolismo , Glicoles de Propileno/farmacología , Receptores de Lisoesfingolípidos/agonistas , Síndrome de Rett/tratamiento farmacológico , Síndrome de Rett/metabolismo , Esfingosina/análogos & derivados , Animales , Astrocitos/citología , Astrocitos/metabolismo , Factor Neurotrófico Derivado del Encéfalo/deficiencia , Muerte Celular/efectos de los fármacos , Muerte Celular/fisiología , Células Cultivadas , Modelos Animales de Enfermedad , Agonistas de Aminoácidos Excitadores/toxicidad , Femenino , Clorhidrato de Fingolimod , Inmunosupresores/farmacología , Sistema de Señalización de MAP Quinasas/efectos de los fármacos , Sistema de Señalización de MAP Quinasas/fisiología , Proteína 2 de Unión a Metil-CpG/genética , Ratones , Actividad Motora/efectos de los fármacos , Actividad Motora/fisiología , N-Metilaspartato/toxicidad , Neuronas/citología , Neuronas/metabolismo , Técnicas de Cultivo de Órganos , Embarazo , Síndrome de Rett/genética , Esfingosina/farmacologíaRESUMEN
Mice mutant for the presynaptic protein Bassoon develop epileptic seizures and an altered pattern of neuronal activity that is accompanied by abnormal enlargement of several brain structures, with the strongest size increase in hippocampus and cortex. Using manganese-enhanced magnetic resonance imaging, an abnormal brain enlargement was found, which is first detected in the hippocampus 1 month after birth and amounts to an almost 40% size increase of this structure after 3 months. Stereological quantification of cell numbers revealed that enlargement of the dentate gyrus and the hippocampus proper is associated with larger numbers of principal neurons and of astrocytes. In search for the underlying mechanisms, an approximately 3-fold higher proportion of proliferation and survival of new-born cells in the dentate gyrus was found to go hand in hand with similarly larger numbers of doublecortin-positive cells and reduced numbers of apoptotic cells in the dentate gyrus and the hippocampus proper. Enlargement of the hippocampus and of other forebrain structures was accompanied by increased levels of brain-derived neurotrophic factor (BDNF). These data show that hippocampal overgrowth in Bassoon-mutant mice arises from a dysregulation of neurogenesis and apoptosis that might be associated with unbalanced BDNF levels.
Asunto(s)
Apoptosis/fisiología , Factor Neurotrófico Derivado del Encéfalo/metabolismo , Giro Dentado/embriología , Proteínas del Tejido Nervioso/metabolismo , Neurogénesis/fisiología , Animales , Astrocitos/metabolismo , Proliferación Celular , Supervivencia Celular/fisiología , Giro Dentado/diagnóstico por imagen , Proteínas de Dominio Doblecortina , Imagen por Resonancia Magnética , Ratones , Ratones Mutantes , Proteínas Asociadas a Microtúbulos/genética , Proteínas Asociadas a Microtúbulos/metabolismo , Proteínas del Tejido Nervioso/genética , Neuronas/metabolismo , Neuropéptidos/genética , Neuropéptidos/metabolismo , Tamaño de los Órganos/genética , RadiografíaRESUMEN
UNLABELLED: Cutaneous carcinomas are the most frequent malignant tumors, the majority of them being located on the face, scalp and back. AIM: To assess the clinical presentation and pathology aspects of the patients with face skin carcinomas admitted to our clinic. MATERIAL AND METHODS: The retrospective study was carried out on a series of 308 patients diagnosed and treated for cutaneous carcinoma of the face in the Department of Oral and Facial Surgery of lasi over a period of 5 years (January 2006 - December 2010). The following parameters were analyzed: demographic data, size and location of the tumor, clinical presentation, and pathology aspects. RESULTS: Basal cell carcinoma accounted for 75.97% of the cases, the nodular, superficial and morphea types being the most common. As to the microscopic aspects, the nodular/solid, superficial, and basosquamous (metatypical) types were the most frequent. The squamous-cell carcinoma represented 18.18%, mainly in the ulcero-vegetant and nodular forms. The moderately and well differentiated forms prevailed. Carcinomas of the skin adnexes as well as Merkel cell carcinomas were the most rare (4.22% and 0.65%, respectively). CONCLUSIONS: The face is the most common location of the cutaneous carcinomas requiring early diagnosis and treatment as a key factor to favorable long term outcome.
Asunto(s)
Carcinoma Basocelular/patología , Carcinoma Basoescamoso/patología , Carcinoma de Células de Merkel/patología , Carcinoma de Células Escamosas/patología , Neoplasias Faciales/patología , Neoplasias Cutáneas/patología , Anciano , Anciano de 80 o más Años , Carcinoma Basocelular/epidemiología , Carcinoma Basocelular/cirugía , Carcinoma Basoescamoso/epidemiología , Carcinoma Basoescamoso/cirugía , Carcinoma de Células de Merkel/epidemiología , Carcinoma de Células de Merkel/cirugía , Carcinoma de Células Escamosas/epidemiología , Carcinoma de Células Escamosas/cirugía , Neoplasias Faciales/epidemiología , Neoplasias Faciales/cirugía , Femenino , Humanos , Incidencia , Masculino , Persona de Mediana Edad , Estudios Retrospectivos , Rumanía/epidemiología , Neoplasias Cutáneas/epidemiología , Neoplasias Cutáneas/cirugía , Resultado del TratamientoRESUMEN
Loss of heterozygosity (LOH) of the entire chromosome 10 is the most frequent genetic alteration in human glioblastoma (GBM). In addition to PTEN/MMAC1 on 10q23.3, clustering of partial deletion break-points on 10q25.3-26.1 points to a second suppressor locus. The proposed target gene DMBT1 was not confirmed. By somatic deletion mapping of this region, we identified the complementary DNA encoding the human homologue of rat orphan G protein-coupled receptor GPR26. GPR26 is highly expressed in fetal and adult brain, but frequently reduced or absent in glioma cells and biopsies, due to de novo methylation of its 5' CpG island. Silencing of GPR26 was reversed with 5-aza-deoxycytidine and the histone deacetylase inhibitor trichostatin A. Furthermore, overexpression of GPR26 in HEK and in U87 glioma cells increased intracellular cAMP concentration which is considered to induce astrocytic differentiation. Interestingly, we observed concomitant silencing of GPR26 with O6-methylguanine-DNA methyl transferase (MGMT), a DNA repair gene co-localized on 10q25.3-26.1 (p=0.0001). We conclude that epigenetic silencing is a common mechanism in malignant gliomas that simultaneously inactivates MGMT and GPR26. The 10q25.3-26.1 region may contain an important epigenetic pathway in brain tumorigenesis.
Asunto(s)
Neoplasias Encefálicas/genética , Cromosomas Humanos Par 10/genética , Silenciador del Gen , Glioma/genética , Receptores Acoplados a Proteínas G/genética , Secuencia de Aminoácidos , Secuencia de Bases , Northern Blotting , Citometría de Flujo , Humanos , Datos de Secuencia Molecular , Análisis de Secuencia por Matrices de Oligonucleótidos , Reacción en Cadena de la Polimerasa de Transcriptasa InversaRESUMEN
Tenascin-C (TNC) expression is known to correlate with malignancy in glioblastoma (GBM), a highly invasive and aggressive brain tumor that shows limited response to conventional therapies. In these malignant gliomas as well as in GBM cell lines, we found Notch2 protein to be strongly expressed. In a GBM tumor tissue microarray, RBPJk protein, a Notch2 cofactor for transcription, was found to be significantly coexpressed with TNC. We show that the TNC gene is transactivated by Notch2 in an RBPJk-dependent manner mediated by an RBPJk binding element in the TNC promoter. The transactivation is abrogated by a Notch2 mutation, which we detected in the glioma cell line Hs683 that does not express TNC. This L1711M mutation resides in the RAM domain, the site of interaction between Notch2 and RBPJk. In addition, transfection of constructs encoding activated Notch2 or Notch1 increased endogenous TNC expression identifying TNC as a novel Notch target gene. Overexpression of a dominant negative form of the transcriptional coactivator MAML1 or knocking down RBPJk in LN319 cells led to a dramatic decrease in TNC protein levels accompanied by a significant reduction of cell migration. Because addition of purified TNC stimulated glioma cell migration, this represents a mechanism for the invasive properties of glioma cells controlled by Notch signaling and defines a novel oncogenic pathway in gliomagenesis that may be targeted for therapeutic intervention in GBM patients.
Asunto(s)
Neoplasias Encefálicas/genética , Glioblastoma/genética , Proteína de Unión a la Señal Recombinante J de las Inmunoglobulinas/biosíntesis , Receptor Notch2/biosíntesis , Tenascina/genética , Secuencia de Aminoácidos , Secuencia de Bases , Neoplasias Encefálicas/metabolismo , Neoplasias Encefálicas/patología , Movimiento Celular/fisiología , Glioblastoma/metabolismo , Glioblastoma/patología , Humanos , Proteína de Unión a la Señal Recombinante J de las Inmunoglobulinas/genética , Inmunohistoquímica , Datos de Secuencia Molecular , Oligodendroglioma/genética , Oligodendroglioma/metabolismo , Oligodendroglioma/patología , Regiones Promotoras Genéticas , Receptor Notch2/genética , Receptor Notch2/metabolismo , Elementos de Respuesta , Transducción de Señal , Tenascina/biosíntesis , Activación TranscripcionalRESUMEN
Natural killer (NK) cell-mediated cytolytic activity against tumors requires the engagement of activating NK receptors by the tumor-associated ligands. Here, we have studied the role of NKG2D and natural cytotoxicity receptors (NCRs) in the recognition of human leukemia. To detect as-yet-unknown cell-surface molecules recognized by NCRs, we developed soluble forms of NKp30, NKp44, and NKp46 as staining reagents binding the putative cognate ligands. Analysis of UL16-binding protein-1 (ULBP1), ULBP2, and ULBP3 ligands for NKG2D and of potential ligands for NKp30, NKp44, and NKp46 in healthy hematopoietic cells demonstrated the ligand-negative phenotype of bone marrow-derived CD34(+) progenitor cells and the acquisition of cell-surface ligands during the course of myeloid differentiation. In acute myeloid leukemia (AML), leukemic blasts from approximately 80% of patients expressed very low levels of ULBPs and NCR-specific ligands. Treatment with differentiation-promoting myeloid growth factors, together with interferon-gamma, upregulated cell-surface levels of ULBP1 and putative NCR ligands on AML blasts, conferring an increased sensitivity to NK cell-mediated lysis. We conclude that the ligand-negative/low phenotype in AML is a consequence of cell maturation arrest on malignant transformation and that defective expression of ligands for the activating NKG2D and NCR receptors may compromise leukemia recognition by NK cells.