PETAL LOSS, a trihelix transcription factor gene, regulates perianth architecture in the Arabidopsis flower

Perianth development is specifically disrupted in mutants of the PETAL LOSS (PTL) gene, particularly petal initiation and orientation. We have cloned PTL and show that it encodes a plant-specific trihelix transcription factor, one of a family previously known only as regulators of light-controlled genes. PTL transcripts were detected in the early-developing flower, in four zones between the initiating sepals and in their developing margins. Strong misexpression of PTL in a range of tissues universally results in inhibition of growth, indicating that its normal role is to suppress growth between initiating sepals, ensuring that they remain separate. Consistent with this, sepals are sometimes fused in ptl single mutants, but much more frequently in double mutants with either of the organ boundary genes cup-shaped cotyledon1 or 2. Expression of PTL within the newly arising sepals is apparently prevented by the PINOID auxin-response gene. Surprisingly, PTL expression could not be detected in petals during the early stages of their development, so petal defects associated with PTL loss of function may be indirect, perhaps involving disruption to signalling processes caused by overgrowth in the region. PTL-driven reporter gene expression was also detected at later stages in the margins of expanding sepals, petals and stamens, and in the leaf margins; thus, PTL may redundantly dampen lateral outgrowth of these organs, helping define their final shape.

Mapping cortical change in Alzheimer's disease, brain development, and schizophrenia

This paper describes algorithms that can identify patterns of brain structure and function associated with Alzheimer's disease, schizophrenia, normal aging, and abnormal brain development based on imaging data collected in large human populations. Extraordinary information can be discovered with these techniques: dynamic brain maps reveal how the brain grows in childhood, how it changes in disease, and how it responds to medication. Genetic brain maps can reveal genetic influences on brain structure, shedding light on the nature-nurture debate, and the mechanisms underlying inherited neurobehavioral disorders. Recently, we created time-lapse movies of brain structure for a variety of diseases. These identify complex, shifting patterns of brain structural deficits, revealing where, and at what rate, the path of brain deterioration in illness deviates from normal. Statistical criteria can then identify situations in which these changes are abnormally accelerated, or when medication or other interventions slow them. In this paper, we focus on describing our approaches to map structural changes in the cortex. These methods have already been used to reveal the profile of brain anomalies in studies of dementia, epilepsy, depression, childhood and adult-onset schizophrenia, bipolar disorder, attention-deficit/ hyperactivity disorder, fetal alcohol syndrome, Tourette syndrome, Williams syndrome, and in methamphetamine abusers. Specifically, we describe an image analysis pipeline known as cortical pattern matching that helps compare and pool cortical data over time and across subjects. Statistics are then defined to identify brain structural differences between groups, including localized alterations in cortical thickness, gray matter density (GMD), and asymmetries in cortical organization. Subtle features, not seen in individual brain scans, often emerge when population-based brain data are averaged in this way. Illustrative examples are presented to show the profound effects of development and various diseases on the human cortex. Dynamically spreading waves of gray matter loss are tracked in dementia and schizophrenia, and these sequences are related to normally occurring changes in healthy subjects of various ages. (C) 2004 Published by Elsevier Inc.

Insertion/deletion polymorphism of the angiotensin converting enzyme gene and loss of the insertion allele in aldosterone-producing adenoma

The genetic mechanisms responsible for the formation of adrenocortical adenomas which autonomously produce aldosterone are largely unknown, The adrenal renin-angiotensin system has been implicated in the pathophysiology of these tumours, Angiotensin-converting enzyme (ACE) catalyses the generation of angiotensin II, and the insertion/deletion (I/D) polymorphism of the ACE gene regulates up to 50% of plasma and cellular ACE variability in humans. We therefore examined the genotypic and allelic frequency distributions of the ACE gene I/D polymorphism in 55 patients with aldosterone-producing adenoma, APA, (angiotensin-unresponsive APA n = 28, angiotensin-responsive APA n = 27), and 80 control subjects with no family history of hypertension, We also compared the ACE gene I/D polymorphism allelic pattern in matched tumour and peripheral blood DNA in the 55 patients with APA, The frequency of the D allele was 0.518 and 0.512 and the I allele was 0.482 and 0.488 in the APA and control subjects respectively, Genotypic and allelic frequency analysis found no significant differences between the groups, Examination of the matched tumour and peripheral blood DNA samples revealed the loss of the insertion allele in four of the 25 patients who were heterozygous for the ACE I/D genotype. The I/D polymorphism of the ACE gene does not appear to contribute to the biochemical and phenotypic characteristics of APA, however, the deletion of the insertion allele of the ACE gene I/D polymorphism in 16% of aldosterone-producing adenomas may represent the loss of a tumour suppressor gene/s or other genes on chromosome 17q which may contribute to tumorigenesis in APA.

Chemokines in human periodontal disease tissues

An immunoperoxidase technique was used to examine IP-10 (interferon-gamma inducible protein 10), RANTES (regulated on activation normal T cell expressed and secreted), MCP-1 (monocyte chemoattractant protein-1), and MIP-1alpha (macrophage inflammatory protein-1alpha) in gingival biopsies from 21 healthy/gingivitis and 26 periodontitis subjects. The samples were placed into 3 groups according to the size of infiltrate. MIP-1alpha+ cells were more abundant than the other chemokines with few MCP-1+ cells. The mean percent MIP-1alpha+ cells was higher than the percent MCP-1+ cells (P = 0.02) in group 2 (intermediate size infiltrates) lesions from periodontitis subjects, other differences not being significant due to the large variations between tissue samples. Analysis of positive cells in relation to CD4/CD8 ratios showed that with an increased proportion of CD8+ cells, the mean percent MIP-1alpha+ cells was significantly higher in comparison with the mean percent RANTES+ and MCP-1+ cells (P < 0.015). Endothelial cells were MCP-1+ although positive capillaries were found on the periphery of infiltrates only. Keratinocyte expression of chemokines was weak and while the numbers of healthy/gingivitis and periodontitis tissue sections positive for IP-10, RANTES and MCP-1 reduced with increasing inflammation, those positive for MIP-1alpha remained constant for all groups. In conclusion, fewer leucocytes expressed MCP-1 in gingival tissue sections, however, the percent MIP-1alpha+ cells was increased particularly in tissues with increased proportions of CD8 cells and B cells with increasing inflammation and also in tissues with higher numbers of macrophages with little inflammation. Further studies are required to determine the significance of MIP-1alpha in periodontal disease.

A longitudinal study of interleukin-1 gene polymorphisms and periodontal disease in a general adult population

Background: Cross-sectional studies have demonstrated that a specific polymorphism (allele 2 of both IL-1A +4845 and IL-1B +3954) in the IL-1 gene cluster has been associated with an increased susceptibility to severe periodontal disease and to an increased bleeding tendency during periodontal maintenance. The aim of the present study was to investigate the relationship between IL-1 genotype and periodontitis in a prospective longitudinal study in an adult population of essentially European heritage. Methods: From an ongoing study of the Oral Care Research Programme of The University of Queensland, 295 subjects consented to genotyping for IL-1 allele 2 polymorphisms. Probing depths and relative attachment levels were recorded at baseline, 6, 12, 24, 36, 48 and 60 months using the Florida probe. Periodontitis progression at a given site was defined as attachment loss greater than or equal to2 mm at any observation period during the 5 years of the study and the extent of disease progression determined by the number of sites showing attachment loss. Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans and Prevotella intermedia were detected using ELISA. Results: 38.9% of the subjects were positive for the composite IL-1 genotype. A relationship between the IL-1 positive genotype and increased mean probing pocket depth in non-smokers greater than 50 years of age was found. Further, IL-1 genotype positive smokers and genotype positive subjects with P. gingivalis in their plaque had an increase in the number of probing depths greater than or equal to3.5 mm, There was a consistent trend for IL-1 genotype positive subjects to experience attachment loss when compared with IL-1 genotype negative subjects. Conclusion: The results of this study have shown an interaction of the IL-1 positive genotype with age, smoking and P. gingivalis which suggests that IL-1 genotype is a contributory but non-essential risk factor for periodontal disease progression in this population.

Effects of phosphonate and salicylic acid treatments on anthracnose disease development and ripening of 'Kensington Pride' mango fruit

This study investigated treatment of mango (Mangifera indica L.) fruit with 2 host defence-promoting compounds for suppression of anthracnose disease (Colletotrichum gloeosporioides). Cultivar 'Kensington Pride' fruit were treated at concentrations of up to 1000 mg/L with either potassium phosphonate or salicylic acid. Applications were by various combinations of pre- and postharvest dips and vacuum infiltration. Postharvest treatments at up to 2000 mg/L salicylic acid were evaluated in a second fruiting season. Fruit were either uninoculated or inoculated with the fungal pathogen. Colour, firmness and disease-severity were assessed during shelf life at 23 degreesC. There were no significant (P>0.05) effects of potassium phosphonate or salicylic acid on anthracnose disease severity in the first season. Moreover, phosphonate or salicylic acid treatment did not significantly affect fruit colour or firmness changes. There were significant (P

Significance of gaseous nitrogen loss from a tropical dairy pasture fertilised with urea

This paper reports a study in the wet tropics of Queensland on the fate of urea applied to a dairy pasture in the absence of grazing animals. A nitrogen balance was conducted in cylindrical plots with N-15-labelled urea, and ammonia volatilisation was determined using a mass balance micrometeorological method. The pasture plants took up 42% of the applied nitrogen in the 98 days between fertiliser application and harvest. At harvest 18% of the applied nitrogen was found in the soil, and 40% was lost from the plant-soil system. The micrometeorological study showed that 20% of the unrecovered nitrogen was lost by ammonia volatilisation. As there was no evidence for leaching or runoff losses it was concluded that the remaining 20% of the applied nitrogen was lost by denitrification. It is evident from these results that fertiliser nitrogen is not being used efficiently on dairy pastures, and that practices need to be changed to conserve fertiliser nitrogen and reduce contamination of the environment.

Apoptosis in the pathogenesis of renal disease with a focus on tubulointerstitial injury

Renal cell apoptosis is important not only in normal physiological conditions of the kidney but also in pathological processes. In normal renal development, it removes unwanted, damaged or harmful cells, and in the healthy adult kidney, it maintains cellular homeostasis by regulating the balance between cell proliferation and cell loss. The apoptotic process has now been described in the pathogenesis and prognosis of certain renal diseases with both beneficial and detrimental roles. It causes deletion of cells intrinsic to the kidney after, for example, toxic, ischaemic, immune or radiation damage, and this loss can be destructive and can cause significant reduction of renal function. In contrast, it can control and limit inflammatory processes in both the acute and chronic phases of renal disease. Information on the positive and negative outcomes of renal cell apoptosis, plus the thousands of publications on more general aspects of apoptosis mechanisms, have now presented real opportunities for the development of therapies that selectively delete or protect certain renal cell populations. This review will discuss some of the more general aspects of renal cell apoptosis and then concentrate on the detrimental or beneficial roles of apoptosis in the initiation, progression or resolution of selected, mainly tubulointerstitial, renal diseases.

Disease, habitat fragmentation and conservation

Habitat loss and the resultant fragmentation of remaining habitat is the primary cause of loss of biological diversity. How do these processes affect the dynamics of parasites and pathogens? Hess has provided some important insights into this problem using metapopulation models for pathogens that exhibit 'S-I' dynamics; for example, pathogens such as rabies in which the host population may be divided into susceptible and infected individuals. A major assumption of Hess's models is that infected patches become extinct, rather than recovering and becoming resistant to future infections. In this paper, we build upon this framework in two different ways: first, we examine the consequences of including patches that are resistant to infection; second, we examine the consequences of including a second species of host that can act as a reservoir for the pathogen. Both of these effects are likely to be important from a conservation perspective. The results of both sets of analysis indicate that the benefits of corridors and other connections that allow species to disperse through the landscape far outweigh the possible risks of increased pathogen transmission. Even in the commonest case, where harmful pathogens are maintained by a common reservoir host, increased landscape connectance still allows greater coexistence and persistence of a threatened or endangered host.

Renal pathology of polycystic kidney disease and concurrent hereditary nephritis in Bull Terriers

Objective To describe the renal lesions in Bull Terrier polycystic kidney disease (BTPKD), to confirm that the renal cysts in BTPKD arise from the nephron or collecting tubule, an to identify lesions consistent with concurrent BTPKD and Bull Terrier hereditary nephritis (BTHN). Design Renal tissue from five Bull Terriers with BTPKD and eight control dogs was examined by light and transmission electron microscopy. Clinical data were collected from all dogs, and family history of BTPKD and BTHN for all Bull Terriers. Results In BTPKD the renal cysts were lined by epithelial cells of nephron or collecting duct origin that were usually squamous or cuboidal, with few organelles. They had normal junctional complexes, and basal laminae of varying thicknesses. Glomeruli with small, atrophic tufts and dilated Bowman's capsules, tubular loss and dilation, and interstitial inflammation and fibrosis were common. Whereas the lesions seen in BTHN by light microscope were nonspecific, the presence of characteristic ultrastructural glomerular basement membrane (GMB) lesions and a family history of this disease indicated concurrent BTHN was likely in three of five cases of BTPKD. Conclusion This paper provides evidence that renal cysts in BTPKD are of nephron or collecting duct origin. In addition, GBM lesions are described that strongly suggest that BTPKD and BTHN may occur simultaneously.

Yield response of rice (Oryza sativa L.) genotypes to different types of drought under rainfed lowlands - Part 3. Plant factors contributing to drought resistance

A series of experiments were conducted in drought-prone northeast Thailand to examine the magnitude of yield responses of diverse genotypes to drought stress environments and to identify traits that may confer drought resistance to rainfed lowland rice. One hundred and twenty eight genotypes were grown under non-stress and four different types of drought stress conditions. Under severe drought conditions, the maintenance of PWP of genotypes played a significant role in determining final grain yield. Because of their smaller plant size (lower total dry matter at anthesis) genotypes that extracted less soil water during the early stages of the drought period, tended to maintain higher PWP and had a higher fertile panicle percentage, filled grain percentage and final grain yield than other genotypes. PWP was correlated with delay in flowering (r = -0.387) indicating that the latter could be used as a measure of water potential under stress. Genotypes with well-developed root systems extracted water too rapidly and experienced severe water stress at flowering. RPR which showed smaller coefficient of variation was more useful than root mass density in identifying genotypes with large root system. Under less severe and prolonged drought conditions, genotypes that could achieve higher plant dry matter at anthesis were desirable. They had less delay in flowering, higher grain yield and higher drought response index, indicating the importance of ability to grow during the prolonged stress period. Other shoot characters (osmotic potential, leaf temperature, leaf rolling, leaf death) had little effect on grain yield under different drought conditions. This was associated with a lack of genetic variation and difficulty in estimating trait values precisely. Under mild stress conditions (yield loss less than 50%), there was no significant relationship between the measured drought characters and grain yield. Under these mild drought conditions, yield is determined more by yield potential and phenotype than by drought resistant mechanisms per se. (C) 2002 Elsevier Science B.V. All rights reserved.

Effect of fertilizer placement on nitrogen loss from sugarcane in tropical Queensland

This paper reports on the fate of nitrogen (N) in a first ratoon sugarcane (Saccharum officinarum L.) crop in the wet tropics of Queensland when urea was either surface applied or drilled into the soil 3-4 days after harvesting the plant cane. Ammonia volatilization was measured with a micrometeorological method, and fertilizer N recovery in plants and soil, to a depth of 140 cm, was determined by mass balance in macroplots with N labelled urea 166 and 334 days after fertilizer application. The bulk of the fertilizer and soil N uptake by the sugarcane occurred between fertilizing and the first sampling on day 166. Nitrogen use efficiency measured as the recovery of labelled N in the plant was very low. At the time of the final sampling (day 334), the efficiencies for the surface and subsurface treatments were 18.9% and 28.8%, respectively. The tops, leaves, stalks and roots in the subsurface treatment contained significantly more fertilizer N than the corresponding parts in the surface treatment. The total recoveries of fertilizer N for the plant-trash-soil system on day 334 indicate significant losses of N in both treatments ( 59.1% and 45.6% of the applied N in the surface and subsurface treatments, respectively). Drilling the urea into the soil instead of applying it to the trash surface reduced ammonia loss from 37.3% to 5.5% of the applied N. Subtracting the data for ammonia loss from total loss suggests that losses by leaching and denitrification combined increased from 21.8% and 40.1% of the applied N as a result of the change in method of application. While the treatment resulted in increased denitrification and/or leaching loss, total N loss was reduced from 59.1% to 45.6%, ( a saving of 13.5% of the applied N), which resulted in an extra 9.9% of the applied N being assimilated by the crop.

Acquisition and loss of Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans and Prevotella intermedia over a 5-year period: effect of a triclosan/copolymer dentifrice

Objectives: The present study describes the natural history of Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans and Prevotella intermedia over a 5-year period and the effect of a triclosan/copolymer dentifrice on these organisms in a normal adult population. Material and Methods: Subgingival plaque samples were collected from 504 adult volunteers. Probing pocket depths (PPD) and relative attachment levels were measured using an automated probe. Participants were matched for disease status (CPI), plaque index, age and gender, and allocated to receive either a triclosan/copolymer or placebo dentifrice. Re-examination and subgingival plaque sampling was repeated after 1, 2, 3, 4 and 5 years. P. gingivalis, A. actinomycetemcomitans and P. intermedia were detected and quantitated using an enzyme linked immunosorbent assay. Logistic regression and generalised linear modelling were used to analyse the data. Results: This 5-year longitudinal study showed considerable volatility in acquisition and loss (below the level of detection) of all three organisms in this population. Relatively few subjects had these organisms on multiple occasions. While P. gingivalis was related to loss of attachment and to PPD greater than or equal to3.5 mm, there was no relationship between A. actinomycetemcomitans or P. intermedia and disease progression over the 5 years of the study. Smokers with P. gingivalis had more PPD greater than or equal to3.5 mm than smokers without this organism. There was no significant effect of the triclosan dentifrice on P. gingivalis or A. actinomycetemcomitans . Subjects using triclosan were more likely to have P. intermedia than those not using the dentifrice; however this did not translate into these subjects having higher levels of P. intermedia and its presence was uniform showing no signs of increasing over the course of the study. Conclusion: The present 5-year longitudinal study has shown the transient nature of colonisation with P. gingivalis , A. actinomycetemcomitans and P. intermedia in a normal adult population. The use of a triclosan-containing dentifrice did not lead to an overgrowth of these organisms. The clinical effect of the dentifrice would appear to be independent of its antimicrobial properties.

The effect of a triclosan-containing dentifrice on the progression of periodontal disease in an adult population

Objectives: The aim of the present study was to determine the effect of unsupervised, long-term use of a 0.3% triclosan/2% copolymer dentifrice on the progression of periodontal disease in a general adult population. Methods: Five hundred and four volunteers were enrolled in a double-blind, controlled clinical trial. Participants were matched for disease status, plaque index, age and gender. At the baseline examination, probing pocket depths and relative attachment levels were recorded and participants were assigned to either the test or control group. Re-examinations took place after 6, 12, 24, 36, 48 and 60 months. Subgingival plaque samples were collected at each examination and assayed for Porphyromonas gingivalis , Actinobacillus actinomycetemcomitans and Prevotella intermedia . A generalised linear model was used to analyse the data, with a number of covariates thought to influence the responses included as the possible confounding effects. Results: The triclosan/copolymer dentifrice had a significant effect in subjects with interproximal probing depths greater than or equal to3.5 mm, where it significantly reduced the number of sites with probing depths greater than or equal to3.5 mm at the following examination, when compared with the control group (p

Resistance to Fiji disease in sugar cane: Role of cultivar preference by planthopper vector Perkinsiella saccharicida (Homoptera : Delphacidae)

Fiji disease (FD) of sugar cane caused by Fiji disease virus (FDV) is transmitted by the planthopper Perkinsiella saccharicida Kirkaldy (Hemiptera: Delphacidae). FD is effectively managed by using resistant cultivars, but whether the resistance is for the vector or for the Virus is Unknown. This knowledge would help develop a rapid and reliable glasshouse-based screening method for disease resistance. Sugar cane cultivars resistant, intermediate, and susceptible to FD were screened in a glasshouse, and the relationship between vector preferences and FD incidence was studied. Cultivar preference by nymphs increased with an increase in cultivar susceptibility to FD, but the relationship between adult preference and FD resistance was not significant. There was a positive correlation between the vector population and FD incidence, and the latent period for symptom expression declined with the increase in the vector populations. FD incidence in the glasshouse trial reflected the field-resistance status of sugar cane cultivars with known FD-resistance scores. The results suggest that resistance to FD in sugar cane is mediated by cultivar preference of the plant-hopper vector.