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1.
Sci Rep ; 14(1): 10542, 2024 May 08.
Artículo en Inglés | MEDLINE | ID: mdl-38719895

RESUMEN

We experimentally demonstrate resonance of first-order vector vortex beams (VVB) with a triangular optical cavity. We also show that, due to their symmetry properties, the VVBs commonly known as radial and azimuthal beams do not resonate at the same cavity length, which could be explored to use the triangular resonator as a mode sorter. In addition, an intracavity Pancharatnam phase shifter (PPS) is implemented in order to compensate for any birefringent phase that the cavity mirrors may introduce.

2.
Leukemia ; 29(7): 1543-54, 2015 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-25652738

RESUMEN

Hematopoietic stem and progenitor cells (HSPC), that is, the cell population giving rise not only to all mature hematopoietic lineages but also the presumed target for leukemic transformation, can transmit (adverse) genetic events, such as are acquired from chemotherapy or ionizing radiation. Data on the repair of DNA double-strand-breaks (DSB) and its accuracy in HSPC are scarce, in part contradictory, and mostly obtained in murine models. We explored the activity, quality and molecular components of DSB repair in human HSPC as compared with mature peripheral blood lymphocytes (PBL). To consider chemotherapy/radiation-induced compensatory proliferation, we established cycling HSPC cultures. Comparison of pathway-specific repair activities using reporter systems revealed that HSPC were severely compromised in non-homologous end joining and homologous recombination but not microhomology-mediated end joining. We observed a more pronounced radiation-induced accumulation of nuclear 53BP1 in HSPC relative to PBL, despite evidence for comparable DSB formation from cytogenetic analysis and γH2AX signal quantification, supporting differential pathway usage. Functional screening excluded a major influence of phosphatidylinositol-3-OH-kinase (ATM/ATR/DNA-PK)- and p53-signaling as well as chromatin remodeling. We identified diminished NF-κB signaling as the molecular component underlying the observed differences between HSPC and PBL, limiting the expression of DSB repair genes and bearing the risk of an inaccurate repair.


Asunto(s)
Transformación Celular Neoplásica/patología , Roturas del ADN de Doble Cadena , Reparación del ADN por Unión de Extremidades/genética , Reparación del ADN/genética , Células Madre Hematopoyéticas/metabolismo , Linfocitos/metabolismo , FN-kappa B/metabolismo , Apoptosis , Western Blotting , Ciclo Celular , Proteínas de Ciclo Celular/metabolismo , Proliferación Celular , Células Cultivadas , Citometría de Flujo , Técnica del Anticuerpo Fluorescente , Células Madre Hematopoyéticas/citología , Humanos , Linfocitos/citología , Transducción de Señal
3.
Am J Ophthalmol ; 129(4): 517-20, 2000 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-10764862

RESUMEN

PURPOSE: To document progressive optic nerve cupping and neural rim decrease in a patient with normal intraocular pressures and bilateral autosomal dominant optic nerve colobomas. METHODS: The ophthalmology records, stereoscopic fundus photographs, and visual fields of a 27-year-old woman with familial (autosomal dominant) optic nerve colobomas were reviewed. The appearance of the optic nerves was documented over a 13-year period (1985 to 1998). RESULTS: Despite repeatedly normal intraocular pressures, the patient showed progressive optic nerve cupping and neural rim decrease in both eyes. Visual field testing was available over a 5-year period (1993 to 1998) and was abnormal, but no progression was seen. CONCLUSIONS: This case of progressive cupping and neural rim decrease in a patient with autosomal dominant optic nerve coloboma in both eyes may provide insight into the optic nerve cupping associated with normal tension glaucoma. Careful follow-up of patients with optic disk colobomas or patients is indicated to detect possible optic nerve changes or field loss.


Asunto(s)
Coloboma/genética , Disco Óptico/patología , Enfermedades del Nervio Óptico/diagnóstico , Nervio Óptico/anomalías , Nervio Óptico/patología , Adulto , Progresión de la Enfermedad , Femenino , Fondo de Ojo , Glaucoma de Ángulo Abierto/fisiopatología , Humanos , Presión Intraocular , Enfermedades del Nervio Óptico/fisiopatología , Fotograbar , Campos Visuales
4.
Cancer Chemother Pharmacol ; 65(6): 1039-46, 2010 May.
Artículo en Inglés | MEDLINE | ID: mdl-19701750

RESUMEN

PURPOSE: The chimeric protein BCR-ABL, a constitutively active protein-tyrosine kinase, triggers downstream signalling proteins, such as STAT3, ultimately resulting in the survival of myeloid progenitors in BCR-ABL-positive leukemias. Here, we evaluated the effect of LLL-3, an inhibitor of STAT3 activity, on cell viability and its addictive effects with Imatinib mesylate (IM) treatment in BCR-ABL-positive cells. METHODS: Viability of cell lines was determined using the WST-1 assay in response to drug treatment, either LLL-3 alone or in conjunction with IM. Annexin V-FITC/PI staining, sub-G1 DNA content and Caspase-3/7 activation assays were performed to evaluate apoptosis. RESULTS: LLL-3 treatment decreased cell viability, triggered apoptosis and activated Caspases-3/7 in K562 cells. LLL-3 increases IM treatment to inhibited cell viability and activation of apoptosis in BCR-ABL-positive cell lines. CONCLUSIONS: LLL-3 reduced cell viability and induced apoptosis in K562 cells. Moreover, the observed addictive effects of co-treatment with IM and LLL-3 suggest this combination has therapeutic potential.


Asunto(s)
Antraquinonas/farmacología , Apoptosis/efectos de los fármacos , Proliferación Celular/efectos de los fármacos , Piperazinas/farmacología , Pirimidinas/farmacología , Factor de Transcripción STAT3/antagonistas & inhibidores , Antineoplásicos/farmacología , Benzamidas , Caspasa 3/metabolismo , Caspasa 7/metabolismo , Línea Celular , Línea Celular Tumoral , Supervivencia Celular/efectos de los fármacos , Relación Dosis-Respuesta a Droga , Sinergismo Farmacológico , Activación Enzimática/efectos de los fármacos , Proteínas de Fusión bcr-abl/metabolismo , Humanos , Mesilato de Imatinib , Concentración 50 Inhibidora , Células K562
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