Effect of top soil wettability on water evaporation and plant growth.

In general, agricultural soil surfaces being hydrophilic in nature get easily wetted by water. The water beneath the soil moves through capillary effect and comes to the surface of the soil and thereafter evaporates into the surrounding air due to atmospheric conditions such as sunlight, wind current, temperature and relative humidity. To lower the water loss from soil, an experiment was designed in which a layer of hydrophobic soil was laid on the surface of ordinary hydrophilic soil. This technique strikingly decreased loss of water from the soil. The results indicated that the evaporation rate significantly decreased and 90% of water was retained in the soil in 83 h by the hydrophobic layer of 2 cm thickness. A theoretical calculation based on diffusion of water vapour (gas phase) through hydrophobic capillaries provide a meaningful explanation of experimental results. A greater retention of water in the soil by this approach can promote the growth of plants, which was confirmed by growing chick pea (Cicer arietinum) plants and it was found that the length of roots, height of shoot, number of branches, number of leaves, number of secondary roots, biomass etc. were significantly increased upon covering the surface with hydrophobic soil in comparison to uncovered ordinary hydrophilic soil of identical depth. Such approach can also decrease the water consumption by the plants particularly grown indoors in residential premises, green houses and poly-houses etc. and also can be very useful to prevent water loss and enhance growth of vegetation in semi-arid regions.

PKA signaling drives mammary tumorigenesis through Src.

Protein kinase A (PKA) hyperactivation causes hereditary endocrine neoplasias; however, its role in sporadic epithelial cancers is unknown. Here, we show that heightened PKA activity in the mammary epithelium generates tumors. Mammary-restricted biallelic ablation of Prkar1a, which encodes for the critical type-I PKA regulatory subunit, induced spontaneous breast tumors characterized by enhanced type-II PKA activity. Downstream of this, Src phosphorylation occurs at residues serine-17 and tyrosine-416 and mammary cell transformation is driven through a mechanism involving Src signaling. The phenotypic consequences of these alterations consisted of increased cell proliferation and, accordingly, expansion of both luminal and basal epithelial cell populations. In human breast cancer, low PRKAR1A/high SRC expression defines basal-like and HER2 breast tumors associated with poor clinical outcome. Together, the results of this study define a novel molecular mechanism altered in breast carcinogenesis and highlight the potential strategy of inhibiting SRC signaling in treating this cancer subtype in humans.

Cord blood mononuclear cell cytokine responses in relation to maternal house dust mite allergen exposure.

BACKGROUND: Cord blood mononuclear cells have demonstrated specific immune responses to environmental allergens. OBJECTIVE: To establish whether the nature of this response is related to the level of maternal antenatal exposure to house dust mite (HDM) allergen and, hence, whether antenatal allergen avoidance may have a role in the prevention of allergic sensitization in children. METHODS: Children with a family history of asthma were recruited antenatally as subjects in a randomised controlled trial: the Childhood Asthma Prevention Study. HDM allergen (Der p 1) concentrations were measured in dust collected from the maternal bed at 36 weeks gestation. Cord blood mononuclear cells were stimulated in culture, separately, with phytohaemaglutinin (PHA) and HDM extract. Cytokine IL-4, IL-5, IL-10 and IFN-gamma concentrations in supernatant were measured by ELISA. mRNA signals for these cytokines were measured using RT-PCR. RESULTS: The median concentration of HDM allergen was 18.4 microg/g (interquartile range 7.3-35.3 microg/g). Median concentrations of IL-4, IL-5, IL-10 and IFN-gamma, after PHA stimulation were 4, 19, 401 and 1781 pg/mL, respectively. After HDM allergen stimulation the median concentrations were 0, 0, 20 and 14 pg/mL, respectively. The distribution of mRNA cytokine signals was similar. Neither cytokine protein concentrations nor cytokine mRNA signal levels were correlated with the concentration of HDM allergen in the mothers' beds at 36 weeks gestation. CONCLUSION: These findings do not support the view that the prevention of allergic disease in children requires the institution of HDM avoidance interventions during pregnancy.

Immunohistochemical localisation of ubiquitin and the proteasome in sunflower (Helianthus annuus cv. Giganteus).

This study provides an immunohistochemical demonstration of the involvement of the ubiquitin- and proteasome-dependent pathway during differentiation and organogenesis in plants. The localisation of ubiquitin and the proteasome was studied in meristems, leaves, stems and roots of sunflower (Helianthus annuus L. cv. Giganteus). By using a new technique that enhances very low antigen signals, we obtained information on the structural distribution of the ubiquitin- and proteasome-dependent pathway, and of the importance of this pathway during organogenesis and plant development. Ubiquitin and the proteasome showed overall similarities in their cellular localisation. The highest antigenic signal was observed in the root and shoot apical meristems, in leaf primordia and vascular tissue. The cambium showed less expression than the apical meristems. During adventitious root formation in cuttings, no sign of increased expression was observed within dedifferentiating tissue, but as organogenesis progressed, the antigenic signal of ubiquitin and the proteasome gradually increased in the developing roots. Comparison of immunochemical results and Western blots demonstrated that important changes in the cellular antigen signal could only be detected by immunochemistry.

Plant cuticle staining with bismarck brown Y and azure B or toluidine blue O before paraffin extraction.

Transverse paraffin sections of mature greenwood stems of rose (Rosa x hybrida) and flowering dogwood (Cornus florida L.) were stained with Bismarck brown followed by azure B or toluidine blue 0. The Bismarck brown was replaced by thiazin dye metachromasia in all structures except the cuticle which remained brown or yellow. The interface between the cuticle and exterior cell walls of the epidermis was delineated clearly.

Novel fixation of plant tissue, staining through paraffin with alcian blue and hematoxylin, and improved slide preparation.

Onion (Allium cepa) root tips were fixed in a proprietary solution without aldehyde, toxic metals or acetic acid. Fixed specimens were embedded in paraffin, sectioned on a rotary microtome and mounted on detergent-washed slides without adhesive. Slides with ribbon segments affixed were immersed in 0.2% aqueous alcian blue 8GX in screw-capped Coplin jars in a water bath at 50 C for 1 hr. Excess alcian blue was rinsed off under cold running tap water and the slides were immersed in quick-mixed hematoxylin at room temperature for 15 min. Stained slides were deparaffinized, rinsed with isopropanol, air dried, and coverslips were affixed with resin. Thus, the traditional paraffin microtechnique has been modified at all steps from fixation to finishing slides with coverslips.

Spontaneous nodules induce feedback suppression of nodulation in alfalfa.

A small subpopulation of alfalfa (Medicago saliva L.) plants grown without fixed nitrogen can develop root nodules in the absence of Rhizobium. Cytological studies showed that these nodules were organized structures with no inter- or intracellular bacteria but with the histological characteristics of a normal indeterminate nodule. Few if any viable bacteria were recovered from the nodules after surface sterilization, and when the nodular content was used to inoculate alfalfa roots no nodulation was observed. These spontaneous nodules were formed mainly on the primary roots in the region susceptible to Rhizobium infection between 4 and 6 d after seed imbibition. Spontaneous nodules appeared as early as 10 d after germination and emerged at a rate comparable to normal nodules. The formation of spontaneous nodules on the primary root suppressed nodulation in lateral roots after inoculation with R. meliloti RCR2011. Excision of spontaneous nodules at inoculation eliminated the suppressive response. Our results indicate that the presence of Rhizobium is not required for nodule organogenesis and the elicitation of feedback regulation of nodule formation in alfalfa.

The tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone is an active transplacental carcinogen in Syrian golden hamsters.

The tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is a potent carcinogen in adult laboratory rodents. Our previous studies have shown that NNK crosses the placenta in pregnant hamsters and is metabolized into DNA-methylating and clastogenic intermediates by fetal respiratory tract tissues. Based on these findings, we have tested the transplacental carcinogenicity of NNK in this species. Groups of pregnant hamsters were given s.c. injections of single or multiple doses of NNK (cumulative dose range, 50-300 mg/kg) on day 15 (last day of gestation) or on days 13, 14, and 15 of gestation. Within 1 year after treatment, up to 70% of the offspring developed tumors in various organs, including respiratory tract, nasal cavity, adrenal glands, pancreas, and liver. No tumors were found in the control hamsters treated with the vehicle (trioctanoin) alone. The overall tumor incidence was proportional to the cumulative dose. Females had a generally higher tumor incidence than males.

Pathobiology of lung tumors induced in hamsters by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone and the modulating effect of hyperoxia.

Neuroendocrine lung cancer is among the most common types of lung cancers in smokers. We have recently shown that exposure of hamsters to N-nitrosodiethylamine and hyperoxia causes a high incidence of this tumor type. In this study, we show that the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone also causes neuroendocrine lung tumors in hyperoxic hamsters. Animals maintained in ambient air while being treated with 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone developed pulmonary adenomas composed of Clara cells and alveolar type II cells. Pathogenesis experiments provide evidence for the tumors caused by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone in ambient air being derived from Clara cells. In the hyperoxic hamsters, the neuroendocrine carcinogenesis appears to involve two stages: (a) transformation of focal alveolar type II cells into neuroendocrine cells and (b) development of neuroendocrine lung tumors from such foci.

Pulmonary bombesin and calcitonin in hamsters during exposure to hyperoxia and diethylnitrosamine.

Combined exposure of hamsters to 60% hyperoxia and the carcinogen diethylnitrosamine for 6 wk resulted in the development of lung tumors. This was associated with progressive loss of body weight as well as increases in the pulmonary-associated peptides, mammalian bombesin (MB) and immunoreactive calcitonin (iCT). After 3 wk of exposure, multiple bronchial epithelial hyperplastic foci were noted, along with increased lung levels of MB and iCT as well as increased serum levels of MB. At this time, immunocytochemistry revealed the presence of MB and iCT within hyperplastic pulmonary neuroendocrine (PNE) cells. In addition, the localization of MB to alveolar type II cells was noted, along with the presence of lamellar bodies and secretion granules in these cells on electron microscopy. After 6 wk of exposure, distinctive microscopic pulmonary tumorlets were seen. These tumorlets were associated with a marked increase in lung and serum MB, and to a lesser extent lung and serum iCT. At this time, MB and iCT were localized exclusively to these abnormal PNE cell sites. These results, which may have relevance in humans, suggest that endogenous peptides may be important components in the process of development of neuroendocrine cancer.

In vitro morphological changes induced by 4-(methylnitrosamino)-1-(3-pyridyl)-1-(butanone) in fetal hamster respiratory tract tissue.

Previous studies conducted in our laboratories have shown that the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is metabolized by fetal hamster respiratory tissues to form DNA-alkylating and clastogenic intermediates. This study was conducted to explore if morphological changes compatible with such events could be detected. Explants of fetal hamster tracheas and lungs were exposed in vitro to various concentrations of NNK and investigated by light and electron microscopy. The explants demonstrated dose dependent preneoplastic lesions in the trachea, while the lung explants exhibited morphological changes compatible with disturbed production and/or release of surfactant.