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A method, called the silicon plate method, has been developed using a small sampling device with a clean simple process, in order to directly evaluate organic contamination on a silicon wafer surface that came from the cleanroom air. Using this method, the concentration of bis͑2-ethylhexyl͒phthalate on the silicon wafer surface is experimentally shown, for the first time, to reach a steady state which has a relationship with its concentration in the cleanroom air. The experimental results are consistent with those theoretically predicted using the model of multicomponent organic species adsorption-induced contamination; therefore, the silicon plate method is concluded to be effective for evaluating the time-dependent behavior of organic species on the silicon wafer surface.The presence of organic hydrocarbon molecules adsorbed on a silicon wafer surface is widely known to cause a serious problem 1-7 of airborne molecular contamination in advanced electronic device fabrication processes. Various organic species [8][9][10][11][12] have been reported to show a time-dependent change in their concentrations on the silicon wafer surface, this is called the fruit basket phenomenon. 11-17 Some organic species show a sharp peak in their surface concentration on the silicon wafer surface which afterward, tends to decrease, indicating gradual replacement by other organic species. Therefore, organic species seem to compete for the adsorption sites on the silicon wafer surface. In order to experimentally evaluate such timedependent organic contamination on the silicon wafer surface, an appropriate and practical sampling and measurement method is required.The organic contamination on the silicon surface is ordinarily measured using wafer thermal desorption gas chromatograph mass spectrometry ͑WTD-GC-MS͒ 18,19 comprising the following steps: (i) thermal desorption of the organic species from the contaminated silicon wafer surface, (ii) transport of the organic species via the gas phase using a carrier gas stream, (iii) collection of the organic species by an adsorbent solid trap ͑Tenax͒, (iv) thermal desorption of the organic species from the adsorbent solid trap, (v) transport of the organic species to the trap at the entrance of the gas chromatograph mass spectrometer, and (vi) transport of the organic species from the trap to the gas chromatograph-mass spectrometer by heating the trap.However, because the fragments caused by the thermal decomposition of the organic molecules have been detected, 18 the high temperature steps in the WTD-GC-MS method are believed to decrease the yield of the organic species and to make the quantitative analysis complicated. Additionally, and unfortunately, in the complicated and large equipment for the WTD-GC-MS method having the cold wall of the infrared furnace and a very long tube connecting the furnace with the adsorbent solid trap, the organic species thermally desorbed from the silicon wafer can be trapped. Therefore, this ordinary method is considered to have some problems in accuracy.Fo...

This study theoretically and experimentally evaluates the role of the coexisting organic compounds on the time-dependent airborne organic contamination on a silicon wafer surface in the cleanroom air. The maximum contamination and the ratio of the desorption to the adsorption are independently described from each other, using simple equations consisting only of the surface concentrations of the organic compounds on the silicon wafer surface. These parameters are consistent with the experiment using the silicon plate sampling method. Additionally, the suppression of the increase in the surface concentration of bis͑2-ethylhexyl͒phthalate theoretically predicted due to the coexisting organic compounds is experimentally observed. The time-dependent behavior of the airborne organic contamination is concluded to occur following the simple rate theory.

BackgroundThere are some reports about the antitumor effects of statins in these days. Statins decrease the level of cholesterol in the blood by inhibiting 3-hydroxy-3-methylglutaryl-coenzyme A reductase. Inhibition of this enzyme decreases intracellular cholesterol synthesis. Thus, the expression of low-density lipoprotein receptor (LDLr) is increased to import more cholesterol from the bloodstream. In this study, we assessed the effects of statins on the proliferation of prostate cancer cells, and studied the relationship between the expression of LDLr and the effects of statins.MethodsSimvastatin was used in the experiments. We studied the effect of simvastatin on PC-3 and LNCaP cell proliferation using the MTS assay, and evaluated the expression of LDLr after administration of simvastatin by quantitative polymerase chain reaction and Western blotting. Intracellular cholesterol levels in the prostate cancer cells were measured after administration of simvastatin. Furthermore, small interfering RNA (siRNA) was used to knockdown the gene expression of LDLr.ResultsIn PC-3 cells, simvastatin inhibited cell proliferation. In LNCaP cells, only a high concentration of simvastatin (100μM) inhibited cell proliferation. In LNCaP cells, the protein level of LDLr was increased by simvastatin. In PC-3 cells, the protein levels of LDLr were unregulated. In PC-3 cells, but not in LNCaP cells, intracellular cholesterol levels were significantly decreased by simvastatin. After knocking down LDLr expression by siRNA, intracellular cholesterol levels were decreased, and cell proliferation was inhibited by simvastatin in LNCaP cells.ConclusionSimvastatin inhibited prostate cancer cell growth by decreasing cellular cholesterol and could be more effective in androgen-independent prostate cancer, where there is loss of regulation of LDLr expression. LDLr was shown to play an important role in the statin-induced inhibition of prostate cancer cell proliferation. These results suggest that future studies evaluating the cholesterol-lowering effects of statin may lead to new approaches to the prevention and treatment of prostate cancer.

Our results suggest that statins inhibit the proliferation, migration, and invasion of androgen-independent prostate cancer cells by up-regulation of ANXA10. Additionally, it is possible that S100A4 plays a role in these effects. Statins may be beneficial in the prevention and/or treatment of prostate cancer. Prostate 77: 337-349, 2017. © 2016 Wiley Periodicals, Inc.

Serum concentrations of luteinizing hormone (LH), testosterone, prostatic acid phosphatase (PAP) and prostatic specific antigen (PSA) were measured in 16 patients with advanced prostatic cancer before and after treatment with luteinizing hormone-releasing hormone (LHRH) analogue. An initial rise of serum LH and testosterone levels was observed on day 2 of the treatment. Subsequently, serum concentrations of PAP and PSA showed a transient increase on day 5 of the treatment. This indicates that LHRH analogues had better be given in combination with antiandrogens in patients with metastatic carcinoma of the prostate.

Abstract.Statins have become of interest in research due to their anticancer effects. However, the exact mechanism of their anticancer properties remains unclear. The authors previously reported that statins decrease intracellular cholesterol levels in androgen-independent prostate cancer cells. In de novo androgen synthesis, cholesterol is the primary material and certain enzymes have important roles. The present study aimed to determine whether simvastatin alters the expression of androgen synthesis-associated enzymes in androgen-independent prostate cancer cells. A novel combination therapy of statins and other drugs that inhibit the overexpression of enzymes involved in androgen synthesis was explored. The cytotoxicity of simvastatin and meclofenamic acid was assessed in prostate cancer cells using MTS and migration assays. Testosterone and dihydrotestosterone concentrations in the culture medium were measured using liquid chromatography-tandem mass spectrometry. RAC-α-serine/threonine-protein kinase (Akt) phosphorylation was detected by western blot analysis. Following treatment with simvastatin, aldo-keto reductase family 1 member C3 (AKR1C3) expression increased in PC-3 (>60-fold) and LNCaP-LA cells, however not in 22Rv1 cells. Small interfering (si)RNA was used to clarify the effects of AKR1C3 expression. The reduction in AKR1C3 expression in PC-3 cells following siRNA transfection was not associated with basal cell proliferation and migration; however, treatment with simvastatin decreased cell proliferation and migration. The combination of simvastatin and meclofenamic acid, an AKR1C3 inhibitor, further enhanced the inhibition of cell proliferation and migration compared with treatment with either drug alone. Furthermore, treatment with simvastatin attenuated insulin-like growth factor 1-induced Akt activation; however, the combination of simvastatin and meclofenamic acid further inhibited Akt activation. These results suggest that the combination of simvastatin and meclofenamic acid may be an effective strategy for the treatment of castration-resistant prostate cancer.

Abstract. Background