Leapfrogging vortex rings for the 3-dimensional incompressible Euler equations

A classical problem in fluid dynamics concerns the interaction of multiple vortex rings sharing a common axis of symmetry in an incompressible, inviscid $3$-dimensional fluid. Helmholtz (1858) observed that a pair of similar thin, coaxial vortex rings may pass through each other repeatedly due to the induced flow of the rings acting on each other. This celebrated configuration, known as leapfrogging, has not yet been rigorously established. We provide a mathematical justification for this phenomenon by constructing a smooth solution of the 3d Euler equations exhibiting this motion pattern

Expression of LIM kinase 1 is associated with reversible G1/S phase arrest, chromosomal instability and prostate cancer

<p>Abstract</p> <p>Background</p> <p>LIM kinase 1 (LIMK1), a LIM domain containing serine/threonine kinase, modulates actin dynamics through inactivation of the actin depolymerizing protein cofilin. Recent studies have indicated an important role of LIMK1 in growth and invasion of prostate and breast cancer cells; however, the molecular mechanism whereby LIMK1 induces tumor progression is unknown. In this study, we investigated the effects of ectopic expression of LIMK1 on cellular morphology, cell cycle progression and expression profile of LIMK1 in prostate tumors.</p> <p>Results</p> <p>Ectopic expression of LIMK1 in benign prostatic hyperplasia cells (BPH), which naturally express low levels of LIMK1, resulted in appearance of abnormal mitotic spindles, multiple centrosomes and smaller chromosomal masses. Furthermore, a transient G1/S phase arrest and delayed G2/M progression was observed in BPH cells expressing LIMK1. When treated with chemotherapeutic agent Taxol, no metaphase arrest was noted in these cells. We have also noted increased nuclear staining of LIMK1 in tumors with higher Gleason Scores and incidence of metastasis.</p> <p>Conclusion</p> <p>Our results show that increased expression of LIMK1 results in chromosomal abnormalities, aberrant cell cycle progression and alteration of normal cellular response to microtubule stabilizing agent Taxol; and that LIMK1 expression may be associated with cancerous phenotype of the prostate.</p

El derecho a la inscripción por el padre en las técnicas de reproducción asistida en Perú

El presente trabajo, plantea como objetivo general: Analizar por qué se restringe el derecho a la inscripción por el padre en las técnicas de reproducción asistida, Perú - 2021; el cual fue estudiar la voluntad de padres que tomaron la decisión de formar una familia en solitario, debido a que se encuentra una vulneración, al limitar la inscripción legal por el padre en la entidad correspondiente para su posterior reconocimiento en nuestra sociedad; considerando que con este tipo de acciones, el derecho a la identidad de aquellos menores, nacidos por la utilización de técnicas de reproducción asistida, se estaría afectando. Pues ante esta situación, se debieron realizar una serie de procesos ya sea en el ámbito administrativo o judicial para poder tener un reconocimiento de su identidad y así poder gozar de otros derechos. En base a esta investigación, se consideró; por un lado, que estos actos en el registro civil, son una vulneración del derecho a la igualdad debido a que la normativa lo excluye de realizar esta inscripción al no tomar en cuenta solo sus apellidos. Asimismo, la metodología fue de tipo aplicada, desde un enfoque cuantitativo, diseño teoría fundamentada, lo cual permitió a la investigadora estudiar de manera objetiva y asertiva dicha realidad social

Down-regulation of Cdc6, a cell cycle regulatory gene, in prostate cancer

CDC6 plays a critical role in regulation of the onset of DNA replication in eukaryotic cells. We have found that Cdc6 expression is down-regulated in prostate cancer as detected by semiquantitative reverse transcriptase-PCR of prostate cell lines and laser-captured microdissected prostate tissues. This result was substantiated by immunohistochemical analysis of paraffin-embedded tissue sections and immunoblot analysis of benign (BPH-1) and adenocarcinomatous prostatic cells. Furthermore, a 100-fold reduction in the transcription efficiency of the Cdc6 promoter-luciferase construct was noted in the metastatic PC3 cells compared with that in BPH-1 cells. Concentration of the E2F and Oct1 transcription factors that have putative binding sites in the Cdc6 promoter was substantially low in PC3 cells compared with BPH cells. Mutagenesis of the two E2F binding sites on the Cdc6 promoter resulted in increased promoter activity in PC3 cells owing to elimination of the negative regulation by pRb-E2F complex but not to the level of that obtained in BPH cells. We conclude that an altered interaction of transcription factors may be responsible for the down-regulation of Cdc6 transcription in PC3 cells. Our study suggests a potential use of the lack of CDC6 expression as an index of prostate cancer development

Down-regulation of Cdc6, a cell cycle regulatory gene, in prostate cancer

CDC6 plays a critical role in regulation of the onset of DNA replication in eukaryotic cells. We have found that Cdc6 expression is down-regulated in prostate cancer as detected by semiquantitative reverse transcriptase-PCR of prostate cell lines and laser-captured microdissected prostate tissues. This result was substantiated by immunohistochemical analysis of paraffin-embedded tissue sections and immunoblot analysis of benign (BPH-1) and adenocarcinomatous prostatic cells. Furthermore, a 100-fold reduction in the transcription efficiency of the Cdc6 promoter-luciferase construct was noted in the metastatic PC3 cells compared with that in BPH-1 cells. Concentration of the E2F and Oct1 transcription factors that have putative binding sites in the Cdc6 promoter was substantially low in PC3 cells compared with BPH cells. Mutagenesis of the two E2F binding sites on the Cdc6 promoter resulted in increased promoter activity in PC3 cells owing to elimination of the negative regulation by pRb-E2F complex but not to the level of that obtained in BPH cells. We conclude that an altered interaction of transcription factors may be responsible for the down-regulation of Cdc6 transcription in PC3 cells. Our study suggests a potential use of the lack of CDC6 expression as an index of prostate cancer development

Androgen regulates Cdc6 transcription through interactions between androgen receptor and E2F transcription factor in prostate cancer cells

Androgen receptor plays a critical role in the development and maintenance of cancers in the prostate. Earlier, we have shown that Cdc6, a regulatory protein for initiation of DNA replication, is down regulated in androgen-insensitive prostate cancer cells. In this report, we studied the involvement of androgen, mediated through androgen receptor (AR) in regulation of Cdc6 expression. Our results demonstrated that androgen treatment stimulated Cdc6 expression in xenograft tumors and androgen-sensitive prostate cancer cells. We also showed that androgen treatment stimulated Cdc6 transcription through possible interaction of AR with the ARE sequence in the Cdc6 promoter and that the stimulatory effect of androgen required intact E2F binding sites in the promoter. Androgen treatment differentially altered nuclear availability of E2F1 and E2F3, and increased the amount of hypophosphorylated retinoblastoma protein (pRb) in the nucleus in a time dependent fashion. We further showed that AR interacted with E2F transcription factors in a ligand-independent manner and that ligand-bound AR was less efficient in interacting with E2F proteins. DNA-protein interaction assays indicated that androgen treatment altered binding of E2F1 to the Cdc6 promoter in prostate cancer cells. We conclude that AR regulates Cdc6 transcription through interaction with the Cdc6 promoter, and complex formation with E2F1 and E2F3 in a differential manner. (c) 2008 Elsevier B.V. All rights reserved

LIM kinase 1 is essential for the invasive growth of prostate epithelial cells - Implications in prostate cancer

Mammalian LIM kinase 1 (LIMK1) is involved in reorganization of actin cytoskeleton through inactivating phosphorylation of the ADF family protein cofilin, which depolymerizes actin filaments. Maintenance of the actin dynamics in an ordered fashion is essential for stabilization of cell shape or promotion of cell motility depending on the cell type. These are the two key phenomena that may become altered during acquisition of the metastatic phenotype by cancer cells. Here we show that LIMK1 is overexpressed in prostate tumors and in prostate cancer cell lines, that the concentration of phosphorylated cofilin is higher in metastatic prostate cancer cells, and that a partial reduction of LIMK1 altered cell proliferation by arresting cells at G(2)/ M, changed cell shape, and abolished the invasiveness of metastatic prostate cancer cells. We also show that the ectopic expression of LIMK1 promotes acquisition of invasive phenotype by the benign prostate epithelial cells. Our data provide evidence of a novel role of LIMK1 in regulating cell division and invasive property of prostate cancer cells and indicate that the effect is not mediated by phosphorylation of cofilin. Our study correlates with the recent observations showing a metastasis-associated chromosomal gain on 7q11.2 in prostate cancer, suggesting a possible gain in LIMK1 DNA (7q11.23)

Correlates of smoking quit attempts: Florida Tobacco Callback Survey, 2007

<p>Abstract</p> <p>Objective</p> <p>The public health burden of tobacco-associated diseases in the USA remains high, in part because many people's attempts to quit are unsuccessful. This study examined factors associated with having lifetime or recent attempts to quit smoking among current smokers, based on a telephone survey of Florida adults.</p> <p>Methods</p> <p>Data from the 2007 telephone-based Florida Behavioral Risk Factor Surveillance System (BRFSS) and its follow-up survey, the Tobacco Callback Survey, were used to assess determinants of having ever attempted to quit smoking and attempted to quit smoking in the past 12 months. All analyses were conducted using SAS.</p> <p>Results</p> <p>Among 3,560 current smokers, 41.5% reported having tried to quit smoking in the past 12 months while 83.4% reported having ever tried to quit. Having a history of a tobacco-related medical condition was significantly associated with both recent (Adjusted Odds Ratio (AOR) 1.41 [Confidence Interval 1.19–1.65]) and lifetime quit attempts (AOR 1.43 [1.15–1.79]). Greater nicotine dependence and being advised by a physician to quit smoking were also positively associated with lifetime quit attempts.</p> <p>Receipt of healthcare provider advice to quit smoking in the past 12 months and a strong belief that quitting following a long history of regular smoking would not result in health benefits and belief that there are health benefits to quitting smoking were associated with lifetime quit attempts.</p> <p>Conclusion</p> <p>Targeted smoking cessation interventions are needed for smokers with selected medical conditions and with high nicotine dependence. The importance of physician advice in encouraging individuals to quit is further highlighted.</p