143 research outputs found

    Magnetic field effect on the sheath thickness in plasma immersion ion implantation

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    The sheath thickness in plasma immersion ion implantation has been investigated in the presence of a transverse magnetic field. It has been found that the steady-state sheath thickness increases with increasing magnetic field strength. This result is in line with a simplified model of the sheath in which the steady-state sheath thickness is determined by the plasma density and ion velocity at the sheath edge. These results suggest that a magnetic field may be used to control the high-voltage sheath in plasma immersion ion implantation. © 2002 American Institute of Physics.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/70576/2/APPLAB-81-7-1183-1.pd

    Particle Simulation of Plume Flows from an Anode-Layer Hall Thruster

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    Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/76848/1/AIAA-28384-370.pd

    Electron-wall interaction in Hall thrusters

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    Electron-wall interaction effects in Hall thrusters are studied through measurements of the plasma response to variations of the thruster channel width and the discharge voltage. The discharge voltage threshold is shown to separate two thruster regimes. Below this threshold, the electron energy gain is constant in the acceleration region and therefore, secondary electron emission (SEE) from the channel walls is insufficient to enhance electron energy losses at the channel walls. Above this voltage threshold, the maximum electron temperature saturates. This result seemingly agrees with predictions of the temperature saturation, which recent Hall thruster models explain as a transition to space-charge saturated regime of the near-wall sheath. However, in the experiment, the maximum saturation temperature exceeds by almost three times the critical value estimated under the assumption of a Maxwellian electron energy distribution function. The channel narrowing, which should also enhance electron-wall collisions, causes unexpectedly larger changes of the plasma potential distribution than does the increase of the electron temperature with the discharge voltage. An enhanced anomalous crossed-field mobility (near wall or Bohm-type) is suggested by a hydrodynamic model as an explanation to the reduced electric field measured inside a narrow channel. We found, however, no experimental evidence of a coupling between the maximum electron temperature and the location of the accelerating voltage drop, which might have been expected due to the SEE-induced near-wall conductivity.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/87763/2/057104_1.pd

    HNF4alpha Dysfunction as a Molecular Rational for Cyclosporine Induced Hypertension

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    Induction of tolerance against grafted organs is achieved by the immunosuppressive agent cyclosporine, a prominent member of the calcineurin inhibitors. Unfortunately, its lifetime use is associated with hypertension and nephrotoxicity. Several mechanism for cyclosporine induced hypertension have been proposed, i.e. activation of the sympathetic nervous system, endothelin-mediated systemic vasoconstriction, impaired vasodilatation secondary to reduction in prostaglandin and nitric oxide, altered cytosolic calcium translocation, and activation of the renin-angiotensin system (RAS). In this regard the molecular basis for undue RAS activation and an increased signaling of the vasoactive oligopeptide angiotensin II (AngII) remain elusive. Notably, angiotensinogen (AGT) is the precursor of AngII and transcriptional regulation of AGT is controlled by the hepatic nuclear factor HNF4alpha. To better understand the molecular events associated with cyclosporine induced hypertension, we investigated the effect of cyclosporine on HNF4alpha expression and activity and searched for novel HNF4alpha target genes among members of the RAS cascade. Using bioinformatic algorithm and EMSA bandshift assays we identified angiotensin II receptor type 1 (AGTR1), angiotensin I converting enzyme (ACE), and angiotensin I converting enzyme 2 (ACE2) as genes targeted by HNF4alpha. Notably, cyclosporine represses HNF4alpha gene and protein expression and its DNA-binding activity at consensus sequences to AGT, AGTR1, ACE, and ACE2. Consequently, the gene expression of AGT, AGTR1, and ACE2 was significantly reduced as evidenced by quantitative real-time RT-PCR. While RAS is composed of a sophisticated interplay between multiple factors we propose a decrease of ACE2 to enforce AngII signaling via AGTR1 to ultimately result in vasoconstriction and hypertension. Taken collectively we demonstrate cyclosporine to repress HNF4alpha activity through calcineurin inhibitor mediated inhibition of nuclear factor of activation of T-cells (NFAT) which in turn represses HNF4alpha that leads to a disturbed balance of RAS

    Low-temperature plasma treatment induces DNA damage leading to necrotic cell death in primary prostate epithelial cells

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    Background:In recent years, the rapidly advancing field of low-temperature atmospheric pressure plasmas has shown considerable promise for future translational biomedical applications, including cancer therapy, through the generation of reactive oxygen and nitrogen species.Method:The cytopathic effect of low-temperature plasma was first verified in two commonly used prostate cell lines: BPH-1 and PC-3 cells. The study was then extended to analyse the effects in paired normal and tumour (Gleason grade 7) prostate epithelial cells cultured directly from patient tissue. Hydrogen peroxide (H2O2) and staurosporine were used as controls throughout.Results:Low-temperature plasma (LTP) exposure resulted in high levels of DNA damage, a reduction in cell viability, and colony-forming ability. H2O2 formed in the culture medium was a likely facilitator of these effects. Necrosis and autophagy were recorded in primary cells, whereas cell lines exhibited apoptosis and necrosis.Conclusions:This study demonstrates that LTP treatment causes cytotoxic insult in primary prostate cells, leading to rapid necrotic cell death. It also highlights the need to study primary cultures in order to gain more realistic insight into patient response

    Development of sentinel node localization and ROLL in breast cancer in Europe

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    The concept of a precise region in which to find the lymph nodes that drain the lymph directly from the primary tumor site can be traced back to a century ago to the observations of Jamieson and Dobson who described how cancer cells spread from cancer of the stomach in a single lymph node, which they called the â\u80\u9cprimary glandâ\u80\u9d. However, Cabanas was the first in 1977 to realize the importance of this concept in clinical studies following lymphography performed in patients with penile cancer. Thanks to Mortonâ\u80\u99s studies on melanoma in 1992, we began to understand the potential impact of the sentinel lymph node (SN) on the surgical treatment of this type of cancer. The use of a vital dye (blue dye) administered subdermally in the region surrounding the melanoma lesion led to the identification of the sentinel node, and the vital dye technique was subsequently applied to other types of solid tumors, e.g. breast, vulva. However, difficulties in using this technique in anatomical regions with deep lymphatic vessels, e.g. axilla, led to the development of lymphoscintigraphy, started by Alex and Krag in 1993 on melanoma and breast cancer and optimized by our group at European Institute of Oncology (IEO) in Milan in 1996. Today, lymphoscintigraphy is still considered as the most reliable method for the detection of the SN. In 1996, a new method for the localization of non-palpable breast lesion called radioguided occult lesion localization (ROLL) was also developed at IEO. Retrospective and prospective studies have since shown that the ROLL procedure permits the easy and accurate surgical removal of non-palpable breast lesions, overcoming the limitations of previous techniques such as the wire-guided localization. The purpose of this paper is to describe the evolution of SN biopsy and radioguided surgery in the management of breast cancer. We also include a review of the literature on the clinical scenarios in which SN biopsy in breast cancer is currently used, with particular reference to controversies and future prospects
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