Depth of a strong jovian jet from a planetary-scale disturbance driven by storms.

The atmospheres of the gas giant planets (Jupiter and Saturn) contain jets that dominate the circulation at visible levels. The power source for these jets (solar radiation, internal heat, or both) and their vertical structure below the upper cloud are major open questions in the atmospheric circulation and meteorology of giant planets. Several observations and in situ measurements found intense winds at a depth of 24 bar, and have been interpreted as supporting an internal heat source. This issue remains controversial, in part because of effects from the local meteorology. Here we report observations and modelling of two plumes in Jupiter's atmosphere that erupted at the same latitude as the strongest jet (23 degrees N). The plumes reached a height of 30 km above the surrounding clouds, moved faster than any other feature (169 m s(-1)), and left in their wake a turbulent planetary-scale disturbance containing red aerosols. On the basis of dynamical modelling, we conclude that the data are consistent only with a wind that extends well below the level where solar radiation is deposited.

Mutation of the zebrafish glass onion locus causes early cell-nonautonomous loss of neuroepithelial integrity followed by severe neuronal patterning defects in the retina.

Mutation of the glass onion locus causes drastic neuronal patterning defects in the zebrafish retina and brain. The precise stratified appearance of the wild-type retina is absent in the mutants. The glass onion phenotype is first visible shortly after the formation of optic primordia and is characterized by the rounding of cells and disruption of the ventricular surface in the eye and brain neuroepithelia. With exception of the dorsal- and ventral-most regions of the brain, neuroepithelial cells lose their integrity and begin to distribute ectopically. At later stages, the laminar patterning of retinal neurons is severely disrupted. Despite the lack of lamination, individual retinal cell classes differentiate in the glass onion retina. Mosaic analysis reveals that the glass onion mutation acts cell nonautonomously within the retina and brain, as neuroepithelial cell morphology and polarity in these tissues are normal when mutant cells develop in wild-type hosts. We conclude that the glass onion mutation affects cell-cell signaling event(s) involved in the maintenance of the neuroepithelial cell layer shortly after its formation. The disruption of neuroepithelial integrity may be the cause of the neuronal patterning defects following neurogenesis. In addition, the expression of the glass onion phenotype in a subset of neuroepithelial cells as well as its onset following the initial formation of the neuroepithelial sheets indicate the presence of genetically distinct temporal and spatial subdivisions in the development of this histologically uniform tissue.

Expression and distribution of cell-surface proteoglycans in the normal Lewis rat molar periodontium.

Cell-surface proteoglycans participate in several biological functions such as cell cell and cell-matrix interactions, cell adhesion, the binding to various growth factors as co-receptors and repair. To understand better the expression and distribution of cell-surface proteoglycans in the periodontal tissues, an immunohistochemical evaluation of the normal Lewis rat molar periodontium using panels of antibodies for syndecan-1, -2, -4, glypican and betaglycan was carried out. Our results demonstrated the expression and distribution of all proteoglycans in the suprabasal gingival epithelium, soft and hard connective tissues. Both cellular and matrix localization was evident within the various periodontal compartments. The presence of these cell-surface proteoglycans indicates the potential for roles in the process of tissue homeostasis, repair or regeneration in periodontium of which each function requires further study.

Cell surface proteoglycan expression by human periodontal cells.

Cell surface proteoglycans are known to be involved in many functions including interactions with components of the extracellular microenvironment and serve to influence cell shape, adhesion, proliferation, and differentiation. They also can act as co-receptors, to help bind and modify the action of various growth factors and cytokines. Despite their strategic location and relevance to cell function, few studies have considered the nature of the cell surface proteoglycans associated with cells of the periodontium. Due to the structural complexity and multiplicity of cell types in the periodontium, we have selected three different cell lines (gingival connective tissue fibroblast, periodontal ligament fibroblast, and osteoblast) which each represent the unique functions within the periodontium to study the expression of cell surface proteoglycans. We hypothesized that a number of cell surface proteoglycans will be expressed by human periodontal cells and these may be related to the source and function of the cell. Western blotting and RT-PCR methods were used to study the expression of five cell surface proteoglycans (syndecan-1, -2, -4, glypican and betaglycan) in three cell lines of human periodontal cells in vitro. Our results demonstrated the expression of protein cores for syndecan-1 (43 kDa), syndecan-2 (48 kDa), syndecan-4 (35 kDa), glypican (64 kDa), and betaglycan (100-110 kDa). RT-PCR results confirmed that all of these cells produced mRNA for the cell surface proteoglycans under study, of which syndecan-2 showed a significant difference in expression between the periodontal ligament fibroblasts, gingival fibroblasts and osteoblasts. We conclude that the presence of specific cell surface proteoglycans on periodontal cells implies a likely role for these molecules in cell-cell, cell-matrix interactions involved in periodontal disease and/or regeneration of the periodontium, of which they may have distinctive functions related to the source and function of these cells.

Identification of bone morphogenetic proteins 2 and 4 in commercial demineralized freeze-dried bone allograft preparations: pilot study.

BACKGROUND: Demineralized freeze-dried bone allografts (DFDBAs) have been proposed as a useful adjunct in periodontal therapy to induce periodontal regeneration through the induction of new bone formation. The presence of bone morphogenetic proteins (BMPs) within the demineralized matrix has been proposed as a possible mechanism through which DFDBA may exert its biologic effect. However, in recent years, the predictability of results using DFDBA has been variable and has led to its use being questioned. One reason for the variability in tissue response may be attributed to differences in the processing of DFDBA, which may lead to loss of activity of any bioactive substances within the DFDBA matrix. Therefore, the purpose of this investigation was to determine whether there are detectable levels of bone morphogenetic proteins in commercial DFDBA preparations. METHODS: A single preparation of DFDBA was obtained from three commercial sources. Each preparation was studied in triplicate. Proteins within the DFDBA samples were first extracted with 4M guanidinium HCI for seven days at 40 degrees celsius and the residue was further extracted with 4M guanidinium HCL/EDTA for seven days at 40 degrees celsius. Two anti-human BMP-2 and -4 antibodies were used for the detection of the presence of BMP's in the extracts. RESULTS: Neither BMP-2 nor BMP-4 was detected in any of the extracts. When recombinant human BMP-2 and -4 were added throughout the extraction process of DFDBA extraction, not only were intact proteins detected but smaller molecular weight fragments were also noted in the extract. CONCLUSIONS: These results indicate that all of the DFDBA samples tested had no detectable amounts of BMP-2 and -4. In addition, an unknown substance present in the DFDBA may be responsible for degradation of whatever BMPs might be present.

Immediate early gene expression and delayed cell death in limbic areas of the rat brain after kainic acid treatment and recovery in the cold.

Systemic injection of kainic acid (KA) results in characteristic behaviors and programmed cell death in some regions of the rat brain. We used KA followed by recovery at 4 degrees C to restrict damage to limbic structures and compared patterns of immediate early gene (IEG) expression and associated DNA binding activity in these damaged areas with that in spared brain regions. Male Wistar rats were injected with KA (12 mg/kg, i.p.) and kept at 4 degrees C for 5 h. This treatment reduced the severity of behaviors and restricted damage (observed by Nissl staining) to the CA1 and CA3 regions of the hippocampus and an area including the entorhinal cortex. DNA laddering, characteristic of apoptosis, was first evident in the hippocampus and the entorhinal cortex 18 and 22 h after KA, respectively. The pattern of IEG mRNA induction fell into three classes: IEGs that were induced in both damaged and spared areas (c-fos, fos B, jun B, and egr-1), IEGs that were induced specifically in the damaged areas (fra-2 and c-jun), and an IEG that was significantly induced by saline injection and/or the cold treatment (jun D). The pattern of immunoreactivity closely followed that of mRNA expression. Binding to the AP-1 and EGR DNA consensus sequences increased in all three regions studied. This study describes a unique modification of the animal model of KA-induced neurotoxicity which may prove a useful tool for dissecting the molecular cascade that ultimately results in programmed cell death.

Immunohistochemical localization of mast cells and mast cell-nerve interactions in oral lichen planus.

OBJECTIVES: Mast cell mediators are likely to be involved in at least some aspects of the immunopathogenesis of oral lichen planus (OLP). The aim of this project was to map mast cell populations in OLP and identify possible sites of mast cell-nerve interactions. MATERIALS AND METHODS: Monoclonal antibodies specific for tryptase and neurofilaments were used to identify mast cells and nerves respectively in an immunohistochemical study of OLP (n = 25) and normal oral buccal mucosa (NOBM) (n = 13) using a double-labelling protocol. Data analysis used paired t-test, multiway analysis of variance and Wilcoxon rank tests. RESULTS: Morphometric analyses showed the greatest mast cell density in the most superficial of the three depth layers examined in OLP, an increase of 130% compared with NOBM. Mast cells associated with neurofilaments ranged from 21.9% in OLP to 10.2% in NOBM. Mean epithelial thickness was significantly lower in OLP (P < 0.001) but without a strong correlation with mast cell density. CONCLUSIONS: Increased mast cell and mast cell-nerve interactions in OLP suggest both a controlling role over the lesional cell populations and a secondary role to the immune response once this becomes established.

Induction of immediate-early, ornithine decarboxylase and antizyme gene expression in the rat small intestine after transient ischaemia.

The expression of the immediate early genes (IEG)s c-fos, c-jun and zif/268, and the genes coding for ornithine decarboxylase (ODC) and its regulatory protein antizyme (AZ), was studied in rat small intestine following transient ischemia. The ischemic stimulus for 10 min alone did not alter the expression of these genes. A rapid and transitory induction of all IEG mRNAs occurred in a coordinated manner peaking at 30 min following recirculation and returned to basal levels 3 hr after recirculation. Protein products of the IEGs accumulated in the smooth muscle layer of the intestine by 2-3 hr after recirculation. Expression of both ODC and AZ mRNAs initially decreased to 70% of control levels 1 hr after recirculation but markedly increased at 2 to 4 hr after recirculation. The functional significance of these changes in gene expression in relation to tissue integrity and function after the ischaemia/reperfusion is discussed.

Expression of the genes coding for ornithine decarboxylase and its regulatory protein antizyme in the developing rat brain.

The ontogenic expression of the genes coding for ornithine decarboxylase (ODC) and its inhibitory protein, antizyme (AZ), was studied in the rat brain between embryonic day (E) 16 and postnatal day (P) 66. The level of ODC mRNA in whole brain was maximal at P2 and rapidly declined by P7 to a low level that was maintained into the adult. Levels of AZ mRNA also peaked at P2, and high levels were sustained into the adult. Regional studies indicated that between P2 and P60 ODC mRNA levels declined in the cerebral cortex, hippocampus and brainstem. These changes reflect the ontogenic pattern of protein levels and enzyme activity suggesting control of this enzyme may occur at the level of transcription. The level of AZ mRNA markedly increased in the cerebellum between P10 and P60. The level of ODC and AZ mRNA at P5 was not altered after continuous suppression of ODC enzyme activity by alpha-difluoromethylornithine between P0 and P5. This suggests that ODC gene expression is not subject to product-related feedback inhibition during this period. Immunohistochemical localisation of ODC protein at P5 revealed ubiquitous distribution of immunoreactivity with higher levels in the hippocampus, cerebral cortex and discrete nuclei in the brainstem. ODC protein was undetectable in the adult rat brain.

The induction of immediate early genes in postischemic and transplanted livers in rats. Its relation to organ survival.

The protein products of the immediate early genes (IEG)s have been proposed to play an important role in long-term tissue plasticity such as cell repair or programmed cell death. The expression of liver IEGs was studied following liver ischemia (LI) or OLT in rats. In LI, 60 min of warm ischemia was induced in shunted rats (shunt LI group; 100% survival) and nonshunted rats (nonshunted LI group; poor survival). In OLT, donor livers were transplanted into the recipients within 1 hr (fresh liver OLT group; 100% survival) or after 24 hr of storage using University of Wisconsin solution (preserved liver OLT group; poor survival). Using both models, IEG mRNAs (c-fos and c-jun) were analyzed by Northern blot hybridization at various times before and after reperfusion. The expression of liver IEGs was not induced by warm ischemia and cold preservation alone. Reperfusion of livers following warm ischemia or cold preservation resulted in a distinctly different pattern of gene expression in viable and nonviable livers. In shunted LI and fresh liver OLT groups (viable), c-fos and c-jun mRNAs increased markedly to a peak value within 1-2 hr of reperfusion, returning to basal level by 3 hr. In nonviable livers, the level of these mRNAs was detected continuously at 3 hr of reperfusion in the nonshunted LI model and also at 6 hr after reperfusion in the preserved liver OLT group. Our data suggest that a protracted pattern of expression of c-fos and c-jun in the liver at the early stage of reperfusion might be correlated with the severity of liver transplant-related insults and subsequent graft failure.

Expression of the gene coding for the NR1 subunit of the NMDA receptor during rat brain development.

Expression of the gene coding for the NR1 subunit of the N-methyl-D-aspartate (NMDA)-type of glutamate receptor was investigated in the developing rat brain. Peak NR1 gene expression in the whole brain occurred at approximately postnatal day (P) 10 with a second increase in the adult. To determine the ontogenic expression in the various brain regions, the expression of NR1 at P2, P10 and P60 was compared. The regional studies indicated increased expression at P60 in the cerebellum. In the midbrain and diencephalon, levels of expression at P10 and P60 were higher than at P2, while in the hippocampus, expression at P10 was significantly higher than at either P2 or P60. Expression in the other brain regions was constant over the period studied. These data indicate a region-specific expression of NR1 in the central nervous system during ontogeny.