Mycotoxins and Fungal Damage in Maize Harvested during 1982 in Far North Queensland

A survey for mycotoxins and fungal damage in maize (Zea mays L.) grown during 1982 in Far North Queensland is reported. This season had a rainfall distribution which was typical for the reglon. The 293 samples examined came from 11 1 farms in eight maize-growing districts. The samples were first subjected to rapid screening tests for fungal damage. Aflatoxins B1, B2, G1, G2 ochratoxin A, T-2 toxin, and sterigmatocystin were not detected, but zearalenone was found in 85% of the samples. The concentrations of zearalenone were correlated with the extent of Gibberella zeae cob rot as indicated by the proportion (up to 2%) of kernels in each sample having a reddish-purple discoloration. In four samples the zearalenone concentration exceeded 1 mg kg-1, but the mean ¦ s.d. (n = 293) concentration in all samples was 0.17 ¦ 0.225 mg kg-1. Concentrations were highest in districts with the highest rainfall during the period of maize growth.

Seasonal effects of foliar application of phosphonate on phosphonate translocation, in vitro pollen viability and pollen germination in `Hass' avocado (Persea americana Mill.)

Phosphonate fungicides are used widely in the control of diseases caused by Phytophthora cinnamomi Rands. For the most part phosphonate is seen as a safe to use on crops with phytotoxicity rare. However, recent research has shown that phosphonate has detrimental effects on the floral biology of some indigenous Australian plants. Since phosphonate fungicides are regularly used for the control of Phytophthora root rot in avocados, research was carried out to study the translocation of phosphonate fungicide in 'Hass' trees and any effects on their floral biology. Field-grown trees were sprayed with 0, 0.06 or 0.12 M mono-dipotassium phosphonate (pH 7.2) at summer flush maturity, floral bud break or anthesis. Following treatment, phosphonic acid concentrations were determined in leaves, roots, inflorescence rachi and flowers and in vitro pollen germination and pollen tube growth studied. Phosphonic acid concentration in the roots and floral parts was related to their sink strength at the respective times of application with concentration in roots highest (36.9.mg g±1) after treatment at summer flush maturity and in flowers (234.7 mg g±1) after treatment during early anthesis. Phosphonate at >0.03 M was found to be significantly phytotoxic to in vitro pollen germination and pollen tube growth. However, this rate gave a concentration far in excess of that measured in plant tissues following standard commercial applications of mono-dipotassium phosphonate fungicide. There was a small effect on pollen germination and pollen tube growth when 0.06 and 0.12 M mono-dipotassium phosphonate was applied during early anthesis. However, under favourable pollination and fruit set conditions it is not expected to have commercial impact on tree yield. However, there may be detrimental commercial implications from phosphonate sprays at early anthesis if unfavourable climatic conditions for pollination and fruit set subsequently occur. A commercial implication from this study is that phosphonic acid root concentrations can be elevated and maintained with strategic foliar applications of phosphonate fungicide timed to coincide with peaks in root sink strength. These occur at the end of the spring and summer flushes when shoot growth is relatively quiescent. Additional foliar applications may be advantageous in under high disease-pressure situations but where possible should be timed to minimize overlap with other significant growth events in the tree such as rapid inflorescence, and fruit development and major vegetative flushing.

Algebraic design techniques for reliable stabilization

In this paper we study two problems in feedback stabilization. The first is the simultaneous stabilization problem, which can be stated as follows. Given plantsG_{0}, G_{1},..., G_{l}, does there exist a single compensatorCthat stabilizes all of them? The second is that of stabilization by a stable compensator, or more generally, a "least unstable" compensator. Given a plantG, we would like to know whether or not there exists a stable compensatorCthat stabilizesG; if not, what is the smallest number of right half-place poles (counted according to their McMillan degree) that any stabilizing compensator must have? We show that the two problems are equivalent in the following sense. The problem of simultaneously stabilizingl + 1plants can be reduced to the problem of simultaneously stabilizinglplants using a stable compensator, which in turn can be stated as the following purely algebraic problem. Given2lmatricesA_{1}, ..., A_{l}, B_{1}, ..., B_{l}, whereA_{i}, B_{i}are right-coprime for alli, does there exist a matrixMsuch thatA_{i} + MB_{i}, is unimodular for alli?Conversely, the problem of simultaneously stabilizinglplants using a stable compensator can be formulated as one of simultaneously stabilizingl + 1plants. The problem of determining whether or not there exists anMsuch thatA + BMis unimodular, given a right-coprime pair (A, B), turns out to be a special case of a question concerning a matrix division algorithm in a proper Euclidean domain. We give an answer to this question, and we believe this result might be of some independent interest. We show that, given twon times mplantsG_{0} and G_{1}we can generically stabilize them simultaneously provided eithernormis greater than one. In contrast, simultaneous stabilizability, of two single-input-single-output plants, g0and g1, is not generic.

Study of surface acidity of oxide catalysts by photoacoustic spectroscopy

Photoacoustic spectroscopy has been employed to estimate quantitatively the acid sites on oxide catalysts. The technique involves the measurement of the ratio of intensities of absorption bands due to conjugate bases and acids of indicators adsorbed on the catalyst surface as a function of the amount of added n-butylamine. Basic sites in sodium-impregnated alumina samples have been examined by adsorbing phenolphthalein on these surfaces.

The Interplay Between KSHV-encoded Viral Cyclin and CDK-inhibitors p27Kip1 and p21Cip1 -implications for Viral Lymphomagenesis

Cell division, which leads to the birth of two daughter cells, is essential for the growth and development of all organisms. The reproduction occurs in a series of events separated in time, designated as the cell cycle. The cell cycle progression is controlled by the activity of cyclin-dependent kinases (CDK). CDKs pair with cyclins to become catalytically active and phosphorylate a broad range of substrates required for cell cycle progression. In addition to cyclins, CDKs are regulated by inhibitory and activating phosphorylation events, binding to CDK-inhibitory proteins (CKI), and also by subcellular localization. The control of the CDK activity is crucial in preventing unscheduled progression of the cell cycle with mistakes having potentially hazardous consequences, such as uncontrolled proliferation of the cells, a hallmark of cancer. The mammalian cell cycle is a target of several DNA tumor viruses that can deregulate the host s cell cycle with their viral oncoproteins. A human herpesvirus called Kaposi s sarcoma herpesvirus (KSHV) is implicated in the cause of Kaposi s sarcoma (KS) and lymphoproliferative diseases such as primary effusion lymphomas (PEL). KSHV has pirated several cell cycle regulatory genes that it uses to manipulate its host cell and to induce proliferation. Among these gene products is a cellular cyclin D homologue, called viral cyclin (v-cyclin) that can activate cellular CDKs leading to the phosphorylation of multiple target proteins. Intriguingly, PELs that are naturally infected with KSHV consistently express high levels of CDK inhibitor protein p27Kip1 and still proliferate actively. The aim of this study was to investigate v-cyclin complexes and their activity in PELs, and search for an explanation why CKIs, such as p27Kip1 and p21Cip1 are unable to inhibit cell proliferation in this type of lymphoma. In this study, we found that v-cyclin binds to p27Kip1 in PELs, and confirmed this novel interaction also in the overexpression models. We observed that p27Kip1 associated with v-cyclin was also phosphorylated by a v-cyclin-associated kinase and identified cellular CDK6 as the major kinase partner of v-cyclin responsible for this phosphorylation. Analysis of the p27Kip1 residues targeted by v-cyclin-CDK6 revealed that serine 10 (S10) is the major phosphorylation site during the latent phase of the KSHV replication cycle. This phosphorylation led to the relocalization of p27Kip1 to the cytoplasm, where it is unable to inhibit nuclear cyclin-CDK complexes. In the lytic phase of the viral replication cycle, the preferred phosphorylation site on p27Kip1 by v-cyclin-CDK6 changed to threonine 187 (T187). T187 phosphorylation has been shown to lead to ubiquitin-mediated degradation of p27Kip1 and downregulation of p27Kip1 was also observed here. v-cyclin was detected also in complex with p21Cip1, both in overexpression models and in PELs. Phosphorylation of p21Cip1 on serine 130 (S130) site by v-cyclin-CDK6 functionally inactivated p21Cip1 and led to the circumvention of G1 arrest induced by p21Cip1. Moreover, p21Cip1 phosphorylated by v-cyclin-associated kinase showed reduced binding to CDK2, which provides a plausible explanation why p21Cip1 is unable to inhibit cell cycle progression upon v-cyclin expression. Our findings clarify the mechanisms on how v-cyclin evades the inhibition of cell cycle inhibitors and suggests an explanation to the uncontrolled proliferation of KSHV-infected cells.

p53 and DNA damage checkpoint responses in the human prostate

Prostate cancer is the most common noncutaneous malignancy and the second leading cause of cancer mortality in men. In 2004, 5237 new cases were diagnosed and altogether 25 664 men suffered from prostate cancer in Finland (Suomen Syöpärekisteri). Although extensively investigated, we still have a very rudimentary understanding of the molecular mechanisms leading to the frequent transformation of the prostate epithelium. Prostate cancer is characterized by several unique features including the multifocal origin of tumors and extreme resistance to chemotherapy, and new treatment options are therefore urgently needed. The integrity of genomic DNA is constantly challenged by genotoxic insults. Cellular responses to DNA damage involve elegant checkpoint cascades enforcing cell cycle arrest, thus facilitating damage repair, apoptosis or cellular senescence. Cellular DNA damage triggers the activation of tumor suppressor protein p53 and Wee1 kinase which act as executors of the cellular checkpoint responses. These are essential for genomic integrity, and are activated in early stages of tumorigenesis in order to function as barriers against tumor formation. Our work establishes that the primary human prostatic epithelial cells and prostatic epithelium have unexpectedly indulgent checkpoint surveillance. This is evidenced by the absence of inhibitory Tyr15 phosphorylation on Cdk2, lack of p53 response, radioresistant DNA synthesis, lack of G1/S and G2/M phase arrest, and presence of persistent gammaH2AX damage foci. We ascribe the absence of inhibitory Tyr15 phosphorylation to low levels of Wee1A, a tyrosine kinase and negative regulator of cell cycle progression. Ectopic Wee1A kinase restored Cdk2-Tyr15 phosphorylation and efficiently rescued the ionizing radiation-induced checkpoints in the human prostatic epithelial cells. As variability in the DNA damage responses has been shown to underlie susceptibility to cancer, our results imply that a suboptimal checkpoint arrest may greatly increase the accumulation of genetic lesions in the prostate epithelia. We also show that small molecules can restore p53 function in prostatic epithelial cells and may serve as a paradigm for the development of future therapeutic agents for the treatment of prostate cancer We hypothesize that the prostate has evolved to activate the damage surveillance pathways and molecules involved in these pathways only to certain stresses in extreme circumstances. In doing so, this organ inadvertently made itself vulnerable to genotoxic stress, which may have implications in malignant transformation. Recognition of the limited activity of p53 and Wee1 in the prostate could drive mechanism-based discovery of preventative and therapeutic agents.

Regulation of oxidative-stress responsive genes by arecoline in human keratinocytes

Background and Objective: Arecoline, an arecanut alkaloid present in the saliva of betel quid chewers, has been implicated in the pathogenesis of a variety of inflammatory oral diseases, including oral submucous fibrosis and periodontitis. To understand the molecular b asis of arecoline action in epithelial changes associated with these diseases, we investigated the effects of arecoline on human keratinocytes with respect to cell growth regulation and the expression of stress-responsive genes.Material and Methods:Human keratinocyte cells (of the HaCaT cell line) were treated with arecoline, following which cell viability was assessed using the Trypan Blue dye-exclusion assay, cell growth and proliferation were analyzed using the MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide) and 5-bromo-2-deoxyuridine incorporation assays, cell cycle arrest and generation of reactive oxygen species were examined using flow cytometry, and gene expression changes were investigated using the reverse transcription-polymerase chain reaction technique. The role of oxidative stress, muscarinic acetylcholine receptor and mitogen-activated protein kinase (MAPK) pathways were studied using specific inhibitors. Western blot analysis was performed to study p38 MAPK activation.Results:Arecoline induced the generation of reactive oxygen species and cell cycle arrest at the G1/G0 phase in HaCaT cells without affecting the expression of p21/Cip1. Arecoline-induced epithelial cell death at higher concentrations was caused by oxidative trauma without eliciting apoptosis. Sublethal concentrations of arecoline upregulated the expression of the following stress-responsive genes: heme oxygenase-1; ferritin light chain; glucose-6-phosphate dehydrogenase; glutamate-cysteine ligase catalytic subunit; and glutathione reductase.Additionally, there was a dose-dependent induction of interleukin-1alfa mRNA by arecoline via oxidative stress and p38 MAPK activation. Conclusion:our data highlight the role of oxidative stress in arecoline-mediated cell death, gene regulation and inflammatory processes in human keratinocytes.

Study of surface acidity of oxide catalysts by photoacoustic spectroscopy

Photoacoustic spectroscopy has been employed to estimate quantitatively the acid sites on oxide catalysts. The technique involves the measurement of the ratio of intensities of absorption bands due to conjugate bases and acids of indicators adsorbed on the catalyst surface as a function of the amount of added n-butylamine. Basic sites in sodium-impregnated alumina samples have been examined by adsorbing phenolphthalein on these surfaces.

Epidemiology of symptomatic human rotaviruses in Bangalore and Mysore, India, from 1988 to 1994 as determined by electropherotype, subgroup and serotype analysis

Epidemiology of symptomatic rotaviruses from Bangalore and Mysore in Southern India was investigated. While serotype G3 predominated throughout the 7-year study period from 1988 to 1994 in Bangalore, serotype G1 was more predominant than serotype G3 in Mysore during 1993 and 1994. Serotype G2 strains were either not detected or infrequently observed in both the cities. However, several strains with subgroup I and lsquoshortrsquo RNA pattern that exhibited high reactivity with typing MAbs specific for serotype 2 as well as other serotypes were detected throughout the period. Among the nonserotypeable strains from both cities, several exhibited dual subgroup (SGI+II) or subgroup I specificity and lsquolongrsquo RNA pattern indicating their probable animal origin. Notably, a gradual, yet highly significant reduction in rotavirus gastroenteritis, from 45.3% in 1988 to 1.8% during 1994, was observed in Bangalore in stark contrast to the consistently high (about 34%) incidence of asymptomatic infections among neonates by I321-like G10P11 type strains during the same period. Moreover, I321-like asymptomatic strains were not detected in children with diarrhea.

Functional Analysis of MrpL55, Vig and Mat1 Acting at the Crossroad of Cell Cycle, Transcription and Metabolism Regulation

Cell proliferation, transcription and metabolism are regulated by complex partly overlapping signaling networks involving proteins in various subcellular compartments. The objective of this study was to increase our knowledge on such regulatory networks and their interrelationships through analysis of MrpL55, Vig, and Mat1 representing three gene products implicated in regulation of cell cycle, transcription, and metabolism. Genome-wide and biochemical in vitro studies have previously revealed MrpL55 as a component of the large subunit of the mitochondrial ribosome and demonstrated a possible role for the protein in cell cycle regulation. Vig has been implicated in heterochromatin formation and identified as a constituent of the RNAi-induced silencing complex (RISC) involved in cell cycle regulation and RNAi-directed transcriptional gene silencing (TGS) coupled to RNA polymerase II (RNAPII) transcription. Mat1 has been characterized as a regulatory subunit of cyclin-dependent kinase 7 (Cdk7) complex phosphorylating and regulating critical targets involved in cell cycle progression, energy metabolism and transcription by RNAPII. The first part of the study explored whether mRpL55 is required for cell viability or involved in a regulation of energy metabolism and cell proliferation. The results revealed a dynamic requirement of the essential Drosophila mRpL55 gene during development and suggested a function of MrpL55 in cell cycle control either at the G1/S or G2/M transition prior to cell differentiation. This first in vivo characterization of a metazoan-specific constituent of the large subunit of mitochondrial ribosome also demonstrated forth compelling evidence of the interconnection of nuclear and mitochondrial genomes as well as complex functions of the evolutionarily young metazoan-specific mitochondrial ribosomal proteins. In studies on the Drosophila RISC complex regulation, it was noted that Vig, a protein involved in heterochromatin formation, unlike other analyzed RISC associated proteins Argonaute2 and R2D2, is dynamically phosphorylated in a dsRNA-independent manner. Vig displays similarity with a known in vivo substrate for protein kinase C (PKC), human chromatin remodeling factor Ki-1/57, and is efficiently phosphorylated by PKC on multiple sites in vitro. These results suggest that function of the RISC complex protein Vig in RNAi-directed TGS and chromatin modification may be regulated through dsRNA-independent phosphorylation by PKC. In the third part of this study the role of Mat1 in regulating RNAPII transcription was investigated using cultured murine immortal fibroblasts with a conditional allele of Mat1. The results demonstrated that phosphorylation of the carboxy-terminal domain (CTD) of the large subunit of RNAPII in the heptapeptide YSPTSPS repeat in Mat-/- cells was over 10-fold reduced on Serine-5 and subsequently on Serine-2. Occupancy of the hypophosphorylated RNAPII in gene bodies was detectably decreased, whereas capping, splicing, histone methylation and mRNA levels were generally not affected. However, a subset of transcripts in absence of Mat1 was repressed and associated with decreased occupancy of RNAPII at promoters as well as defective capping. The results identify the Cdk7-CycH-Mat1 kinase submodule of TFIIH as a stimulatory non-essential regulator of transcriptional elongation and a genespecific essential factor for stable binding of RNAPII at the promoter region and capping. The results of these studies suggest important roles for both MrpL55 and Mat1 in cell cycle progression and their possible interplay at the G2/M stage in undifferentiated cells. The identified function of Mat1 and of TFIIH kinase complex in gene-specific transcriptional repression is challenging for further studies in regard to a possible link to Vig and RISC-mediated transcriptional gene silencing.

Deregulation of miR-126 expression in colorectal cancer pathogenesis and its clinical significance

In this study, we investigated the expression profiles and clinicopathological significance of miR-126 in large cohort of patients with colorectal cancers as well the cellular repercussions of miR-126 in colon cancer cells along with its targets in-vitro. Down regulation of miR-126 expression was associated with histological subtypes, peri-neural tumour infiltration, microsatellite instability and pathological staging of colorectal cancers (p<0.05). Low miR-126 expression was also associated with poorer survival in patients with colorectal cancer. Analysis of matched tissues from the same patient revealed that approximately 70% of the tested patients had similar levels of expression of miR-126 in primary cancer and cancer metastases in both lymph node and distant metastases. In addition, induced overexpression of miR-126 showed reduced cell proliferation, increased apoptosis and decreased accumulation of cells in the G0-G1 phase of the colon cancer cells. Furthermore, SW480(+miR-126) cells showed reduced BCL-2 and increased P53 protein expression. To conclude, deregulation of miR-126 in colorectal cancer at the tissue and cellular levels as well as its correlation with various clinicopathological parameters confirm the cancer suppressive role of miR-126 in colorectal cancer.

Hadwiger Number and the Cartesian Product of Graphs

The Hadwiger number eta(G) of a graph G is the largest integer n for which the complete graph K-n on n vertices is a minor of G. Hadwiger conjectured that for every graph G, eta(G) >= chi(G), where chi(G) is the chromatic number of G. In this paper, we study the Hadwiger number of the Cartesian product G square H of graphs. As the main result of this paper, we prove that eta(G(1) square G(2)) >= h root 1 (1 - o(1)) for any two graphs G(1) and G(2) with eta(G(1)) = h and eta(G(2)) = l. We show that the above lower bound is asymptotically best possible when h >= l. This asymptotically settles a question of Z. Miller (1978). As consequences of our main result, we show the following: 1. Let G be a connected graph. Let G = G(1) square G(2) square ... square G(k) be the ( unique) prime factorization of G. Then G satisfies Hadwiger's conjecture if k >= 2 log log chi(G) + c', where c' is a constant. This improves the 2 log chi(G) + 3 bound in [2] 2. Let G(1) and G(2) be two graphs such that chi(G1) >= chi(G2) >= clog(1.5)(chi(G(1))), where c is a constant. Then G1 square G2 satisfies Hadwiger's conjecture. 3. Hadwiger's conjecture is true for G(d) (Cartesian product of G taken d times) for every graph G and every d >= 2. This settles a question by Chandran and Sivadasan [2]. ( They had shown that the Hadiwger's conjecture is true for G(d) if d >= 3).

Soluautomaattien approksimaatioista

Tässä tutkielmassa tarkastelen soluautomaatteja ja niiden yleisesti käytettyj ä keskivertokenttä- ("mean field") ja pariapproksimaatioita. Määrittelen soluautomaatin käsitteen yleisellä tasolla ja kuvailen kolme eri tyypillisesti käytettyä soluautomaattityyppiä, joista kahdesta esimerkkeinä mainitsen John Conwayn tunnetun "Game of Life" -soluautomaatin sekä epidemiologian alalla yleisesti käytetyn hilakontaktiprosessin. Tutkielman toisessa osassa esittelen eri tapoja, joilla soluautomaattien käyttäytymistä voidaan analyyttisesti approksimoida ja karakterisoida, mukaanlukien niin kutsuttu soluautomaatin aktiviteetti (λ) sekä yllämainitut keskivertokenttä- ja pariapproksimaatiot. Kahta jälkimmäistä sovellan hilakontaktiprosessiin, ja vertailen näin saatuja tuloksia.

The effect of viscosity and surface tension on the Taylor instability of the surface of a cavitation bubble*

This paper is devoted to a consideration of the following problem: A spherical mass of fluid of density varrho1, viscosity μ1 and external radius R is surrounded by a fluid of density varrho2 and viscosity μ2.The fluids are immiscible and incompressible. The interface is accelerated radially by g1: to study the effect of viscosity and surface tension on the stability of the interface. By analyzing the problem in spherical harmonics the mathematical problem is reduced to one of solution of the characteristic determinant equation. The particular case of a cavity bubble, where the viscosity μ1 of the fluid inside the bubble is negligible in comparison with the viscosity μ2 of the fluid outside the bubble, is considered in some detail. It is shown that viscosity has a stabilizing role on the interface; and when g1 > T(n − 1) (n + 2)/R2(varrho2 − varrho1) the stabilizing role of both viscosity and surface tension is more pronounced than would result when either of them is taken individually.

Perspektiv på språkprocessering

Automatisk språkprocessering har efter mer än ett halvt sekel av forskning blivit ett mycket viktigt område inom datavetenskapen. Flera vetenskapligt viktiga problem har lösts och praktiska applikationer har nått programvarumarknaden. Disambiguering av ord innebär att hitta rätt betydelse för ett mångtydigt ord. Sammanhanget, de omkringliggande orden och kunskap om ämnesområdet är faktorer som kan användas för att disambiguera ett ord. Automatisk sammanfattning innebär att förkorta en text utan att den relevanta informationen går förlorad. Relevanta meningar kan plockas ur texten, eller så kan en ny, kortare text genereras på basen av fakta i den ursprungliga texten. Avhandlingen ger en allmän översikt och kort historik av språkprocesseringen och jämför några metoder för disambiguering av ord och automatisk sammanfattning. Problemområdenas likheter och skillnader lyfts fram och metodernas ställning inom datavetenskapen belyses.