Correlation Between Time Change in Modulus of Short-Period Geomagnetic Variation and Seismicity in Taiwan

In this study, geomagnetic data of the Lunping observatory from 1993 to 2000 are utilized for computing the amplitude variation of short-period geomagnetic total intensity data, using the complex demodulation method (CD method). In order to compare these time changes with seismicity, earthquakes that occurred within 150 km of Lunping, with magnitude ML greater than 3.0, are located. The total sum of those earthquakes, summed month by month, is correlated with the modulus. After removing seasonal effect, our results show that the modulus of periods 24, 12, and 8 hr reveals a notable change that seems to be related to the total sum of events within the whole study period. One possible precursor is found 6 months prior to the 1999 high seismicity. The modulus for the periods 24, 12, and 8 hr increased gradually from the beginning of 1999 to August 1999. After earthquake occurrence the modulus decreased again to a normal level. We propose that this notable increase might be related to a preparation process for this strong earthquake

Smoking, Green Tea Consumption, Genetic Polymorphisms in the Insulin-Like Growth Factors and Lung Cancer Risk

Insulin-like growth factors (IGFs) are mediators of growth hormones; they have an influence on cell proliferation and differentiation. In addition, IGF-binding protein (IGFBP)-3 could suppress the mitogenic action of IGFs. Interestingly, tea polyphenols could substantially reduce IGF1 and increase IGFBP3. In this study, we evaluated the effects of smoking, green tea consumption, as well as IGF1, IGF2, and IGFBP3 polymorphisms, on lung cancer risk. Questionnaires were administered to obtain the subjects' characteristics, including smoking habits and green tea consumption from 170 primary lung cancer cases and 340 healthy controls. Genotypes for IGF1, IGF2, and IGFBP3 were identified by polymerase chain reaction. Lung cancer cases had a higher proportion of smoking, green tea consumption of less than one cup per day, exposure to cooking fumes, and family history of lung cancer than controls. After adjusting the confounding effect, an elevated risk was observed in smokers who never drank green tea, as compared to smokers who drank green tea more than one cup per day (odds ratio (OR) = 13.16, 95% confidence interval (CI) = 2.96–58.51). Interaction between smoking and green tea consumption on lung cancer risk was also observed. Among green tea drinkers who drank more than one cup per day, IGF1 (CA)19/(CA)19 and (CA)19/X genotypes carriers had a significantly reduced risk of lung cancer (OR = 0.06, 95% CI = 0.01–0.44) compared with IGF1 X/X carriers. Smoking-induced pulmonary carcinogenesis could be modulated by green tea consumption and their growth factor environment

Association between green tea consumption and smoking status with lung cancer risk.

<p>Data were matched by age and gender, calculated by multiple conditional logistic regression and adjusted for exposure to fume of cooking, and family history of lung cancer.</p>1<p>P<0.01,</p>2<p>P = 0.04; P value was adjusted by multiple testing (bonferroni correction).</p

Frequency distribution of specific characteristics by case and control status.

<p>Data were matched by age and gender, calculated by conditional logistic regression.</p>1<p>Two-sided χ² test or Fisher's exact test for discrete variables and paired <i>t</i>-test for continuous variables.</p

The joint effect of cumulative smoking dose with <i>IGF1</i> (CA)_n repeat, <i>IGF2</i> 820, <i>IGFBP3</i> -202 genotypes for lung cancer risk.

<p>Data were matched by age and gender, calculated by multiple conditional logistic regression and adjusted for green tea consumption, exposure to fume of cooking, and family history of lung cancer.</p>1<p>P<0.01,</p>2<p>P = 0.08,</p>3<p>P = 0.03; P value was adjusted by multiple testing (bonferroni correction).</p

Risk of lung cancer in association with <i>IGF1</i> (CA)_n repeat genotype by different status of green tea consumption.

<p>Data were matched by age and gender, calculated by multiple conditional logistic regression and adjusted for pack-years of smoking, exposure to fume of cooking, and family history of lung cancer.</p>1<p>P = 0.03,</p>2<p>P = 0.11; P value was adjusted by multiple testing (bonferroni correction).</p

Genotype frequencies of <i>IGF1</i> (CA)_n repeat, <i>IGF2</i> 820 and <i>IGFBP3</i> -202 among cases and controls.

<p>Data were matched by age and gender, calculated by conditional logistic regression.</p>1<p>Data were calculated by two-sided χ² test.</p>2<p>The probability of the χ² test for Hardy-Weinberg equilibrium in control group.</p

Evolutional change of karyotype with t(8;9)(p22;p24) and HLA-DR immunophenotype in relapsed acute myeloid leukemia

The rare recurrent translocation of (8;9)(p22;p24) with PCM1-JAK2 fusion was recently characterized in diverse hematological malignancies. Most of them are atypical chronic myeloid leukemia (CML) or other myeloproliferative disorders (MPD), and are predominantly in the male. We report a female patient with acute myeloid leukemia (AML) initially presenting with normal karyotype and negative HLA-DR expression who achieved complete remission after standard chemotherapy. The disease relapsed 7 months later with cytogenetic change of t(8;9)(p22;p24). Flow cytometry analysis showed evolutional change of immunophenotype from negative to positive HLA-DR expression and fluorescence in situ hybridization (FISH) analysis demonstrated a PCM1-JAK2 fusion gene. We speculate that the cytogenetic change of t(8;9)(p22;p24) may induce HLA-DR immunophenotypic switch and a coordination of the two evolutional changes may play a role in leukemic cell progression

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field