Phytoalexins and resistance to vascular wilts in tomato

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A sequential test procedure for monitoring a singular safety and efficacy outcome

In this note we describe a modification of the sequential probability ratio test (SPRT) developed for the purpose of “flagging” a significant increase in the mortality rate of a treatment relative to a control while ensuring that double-blinding and the Type I error for the primary test of efficacy, also based on mortality rates, is not compromised. Key words: Interim analysis; safety monitoring; sequential testing. Trop J Pharm Res, December 2003; 2(2): 197-20

A Characterization of Most(More) Powerful Test Statistics with Simple Nonparametric Applications

Data-driven most powerful tests are statistical hypothesis decision-making tools that deliver the greatest power against a fixed null hypothesis among all corresponding data-based tests of a given size. When the underlying data distributions are known, the likelihood ratio principle can be applied to conduct most powerful tests. Reversing this notion, we consider the following questions. (a) Assuming a test statistic, say T, is given, how can we transform T to improve the power of the test? (b) Can T be used to generate the most powerful test? (c) How does one compare test statistics with respect to an attribute of the desired most powerful decision-making procedure? To examine these questions, we propose one-to-one mapping of the term 'Most Powerful' to the distribution properties of a given test statistic via matching characterization. This form of characterization has practical applicability and aligns well with the general principle of sufficiency. Findings indicate that to improve a given test, we can employ relevant ancillary statistics that do not have changes in their distributions with respect to tested hypotheses. As an example, the present method is illustrated by modifying the usual t-test under nonparametric settings. Numerical studies based on generated data and a real-data set confirm that the proposed approach can be useful in practice.Comment: Accepte

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

A Pilot Study of Urokinase-Type Plasminogen Activator (uPA) Overexpression in the Brush Cytology of Patients with Malignant Pancreatic or Biliary Strictures

We have previously demonstrated that uPA is overexpressed in pancreatic tumors. In an attempt to diagnose these tumors earlier, we sought to determine whether uPA could be identified in endoscopic retrograde cholangiopancreatography obtained brushings in patients with malignant pancreatic and biliary strictures. Secondarily, uPA was measured in the serum of this patient population. uPA overexpression was identified in the cytologic tissue in 8 of 11 patients (72.7%). Serum analysis demonstrated a 2-fold higher concentration of uPA in the pancreaticobiliary cancer patients (1.27 versus 0.56 ng/mL; P = .0182). Also, uPA overexpression correlated with serum levels (P < .0001). This study confirms that uPA can be detected in the ERCP cytologically obtained tissue and is frequently present in a higher concentration in the serum of pancreaticobiliary cancer patients. A larger sample size will be required to address its value as a sensitive marker for the diagnosis of pancreatic or biliary cancers