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Previous studies have demonstrated that vegetation‐generated turbulence can enhance erosion rate and reduce the velocity threshold for erosion of non‐cohesive sediment. This study considered whether vegetation‐generated turbulence had a similar influence on natural cohesive sediment. Cores were collected from a black mangrove forest with aboveground biomass and exposed to stepwise increases in velocity. Erosion was recorded through suspended sediment concentration. For the same velocity, cores with pneumatophores had elevated turbulent kinetic energy compared to bare cores without pneumatophores. However, the vegetation‐generated turbulence did not increase bed stress or the rate of resuspension, relative to bare cores. It was hypothesized that the short time‐scale fluctuations associated with vegetation‐generated turbulence were not of sufficient duration to break cohesion between grains, explaining why elevated levels of turbulence associated with the pneumatophores had no impact on the erosion threshold or rate. Mangrove habitat grows by retaining sediment. To restore these systems, it is necessary to understand how vegetation influences the transport and retention of sediment. This study used sediment cores collected from the interior of a mangrove forest to study how the aboveground roots, called pneumatophores, influence hydrodynamic conditions and sediment transport, and in particular the onset and rate of sediment erosion. Individual pneumatophores generate eddies that enhance turbulence, compared to conditions without pneumatophores. In sandy soil, vegetation‐generated turbulence can enhance erosion. However, in this study, vegetation‐generated turbulence did not increase the rate of erosion for natural cohesive (muddy) sediment, suggesting that the mangrove forest interior has naturally greater resistance to erosion and sediment loss. For the same velocity, cores with pneumatophores had higher turbulent kinetic energy (TKE) compared to cores without pneumatophoresUnlike sands, the inception of erosion and erosion rates for cohesive sediment were better predicted by bed shear stress than by TKEModelers should parameterize erosion within vegetation differently for cohesive and non‐cohesive sediment For the same velocity, cores with pneumatophores had higher turbulent kinetic energy (TKE) compared to cores without pneumatophores Unlike sands, the inception of erosion and erosion rates for cohesive sediment were better predicted by bed shear stress than by TKE Modelers should parameterize erosion within vegetation differently for cohesive and non‐cohesive sediment

This article focuses on the technique of decomposing a system as a tool for the analysis of large and complex systems. In order to simplify the analysis, and often as a matter of necessity, it is natural in a model or a theory to not take certain variables explicitly into account or to hold them constant, even though they may be related to the phenomenon under analysis. Examples of this kind of simplification are easy to find; economists may study some aspects of the behavior of a country's internal economy without regard to its exchanges with the rest of the world, or social scientists may analyze the behavior of a group without regard to other roles played by the group members in other contexts. The basic principles at work in this type of approximation are well illustrated by the familiar kinetic model of a chemical reaction. The differential equations of these models describe the time variations of the chemical concentrations of the various constituents of the reaction. Typically, these equations rely on two types of simplifying assumptions.

Keratinocytes not only produce vitamin D3in response to ultraviolet B light (UVB) and convert 25-hydroxyvitamin D3to 1α,25-dihydroxyvitamin D3(1,25(OH)2D) but also possess the vitamin D receptor (VDR) and respond to 1,25(OH)2D. We characterized the regulation of the expression of the VDR gene in primary human keratinocytes following UVB irradiation. We report a marked dose-dependent down-regulation of the VDR mRNA and protein within a few hours after irradiation. This occurs independently ofde novoprotein synthesis and is not due to a change in the half-life of the VDR mRNA. Interestingly, treatment of the cells with sodium salicylate, caffeic acid phenethyl ester and tosylphenylchloromethylketone inhibited this down-regulation. Our results strongly suggest the existence of a feedback mechanism in that UVB initiates vitamin D synthesis in keratinocytes and at the same time limits VDR abundance. They also provide a rational explanation for the reported lack of any additive effect between 1,25(OH)2D and UVB phototherapy in the treatment of psoriasis.

Wild-type p53 (wt-p53) negatively controls cell cycle progression after cellular stress mediating either a temporary growth arrest or apoptosis, depending on the cell type and nature of the cellular stress. The aberrant proliferation which is characteristic of tumor cells may be suppressed by exogenous wt-p53 and appears to depend strongly on the level of reexpression. We performed retroviral-mediated gene transfer of wt-p53 into a human squamous cell carcinoma cell line from the head and neck region (A253 cell line) lacking endogenous p53. This allowed us to study the effect of wt-p53 on the malignant phenotype and on the response to the DNA damaging agent ultraviolet B (UVB). Restoration of wt-p53 in malignant keratinocytes suppressed tumorigenicity in nude mice although p53-reconstituted cells eventually formed small tumors with long latency. Cells derived from these tumors showed reduced expression of wt-p53. Exogenous wt-p53 increased baseline mRNA expression of the small proline rich proteins 1 and 2, consistent with a prodifferentiating effect. After exposure to a biological UVB dose, only p53-positive A253 cells underwent an early and transient G1 arrest. Both p53-positive and -negative A253 cells displayed a late G2 delay/arrest. We conclude that reexpression of wt-p53 in squamous cell carcinoma A253 cells decreases their malignant phenotype and reestablishes a G1 checkpoint after UVB.

Despite the many developments in the area of sexual dysfunction, rehabilitation settings seldom investigate the remaining sexual function following spinal cord injury, or offer differential diagnoses of sexual dysfunction in spinal cord injured men. This article attempts to show how sexual rehabilitation should begin with a thorough assessment of the sexual function of paraplegic and tetraplegic men. Assessment includes a basic neurological examination of the perineal area and an extended clinical interview on sexual function and visceral function. The interpretation of patient evaluation is discussed in terms of a classification system adapted to sexual purposes and in terms of the differential diagnoses between sexual dysfunctions of organic, and those of predominantly psychogenic origin in the spinal cord injured patient. The organic or psychogenic contribution is discussed in terms of sophisticated procedures, where assessment of nocturnal penile tumescence (NPT) is critically evaluated and where alternatives such as urodynamic findings and skin potentials are discussed. Treatment strategies, such as intracavernous injections and cognitive-behavioural strategies adapted to different lesion types, are discussed.

The MAGE1 gene codes for an antigen recognized on melanoma cell line MZ2-MEL by autologous cytolytic T lymphocytes. It is expressed in a number of tumors of different histological origins, but not in normal tissues except in testis. The MAGE1 promoter region was analyzed by performing transient transfections in MZ2-MEL cells with luciferase reporter plasmids. A fragment extending from nucleotide -792 to +118 exhibited high transcriptional activity. By deletional analysis of this fragment, we identified five activating regions designated C, A, B', B, and D. The activity of region A depends on the presence of region B' and vice versa. Two inverted Ets motifs contained in regions B' and B were found to drive 90% of the activity of the MAGE1 promoter in MZ2-MEL cells. Electrophoretic mobility shift assays performed with a nuclear extract from MZ2-MEL cells and with competitor oligonucleotides containing an Ets consensus site showed that nuclear proteins bind to the Ets motif of regions B' and B. Similar experiments suggested that region A binds transcription factors of the Sp1 family. The MAGE1 promoter was found to exert transcriptional activity in tumor cells where the MAGE1 gene is not expressed, suggesting that other mechanisms, such as demethylation, may contribute to the tumor-specific expression of the gene.

The purpose of this studywas to provide additional evidence that in the lesions of acute necrotizing ulcerative gingivitis (ANUG), spirochetes and other microorganisms are capable of invading the nonnecrotic lamina propria of affected gingivae. Biopsies from eight patients with pathognomonic signs of ANUG were obtained under local anesthesia and processed for light and transmission electron microscopy. The results indicated that spirochetes and other bacteria are capable of penetrating the viable connective tissues of the lamina propria. The four zones of the ANUG lesion as first described by Listgarten were observed without difficulty. The maximum depth of bacterial infiltration into the lamina propria ranged from 155 to 400 microns from the nearest epithelial basal lamina. The histologic picture of the ANUG lesion did not always conform to the acute clinical manifestations.

Precise diagnoses are seldom made upon complaints of sexual dysfunction by spinal cord injured men. The dysfunction is inevitably attributed to the neurological condition and available treatments are offered with little knowledge of the individual residual capacity or other contributing factors. Current practice emphasizes these treatment approaches, but the high rejection rate associated with the most widely used technique of intracavernous injections suggests that remaining sexual function should also be investigated. This study explores remaining function using physiological recording techniques and classifying the subjects according to the innervation of the reproductive system. The results show that, with objective measurements and proper classification of the subjects, 100% of individuals with high lesions maintain penile responses to reflexogenic stimulation and up to 90% of those with lower lesions maintain penile responses to psychogenic stimulation. These latter subjects also show naturally occurring emissions in 100% of the cases when they suffer from lesions to the conus terminalis and when they use psychogenic stimulation as a means of inducing erection and emission. Results from subjective reports reveal that spinal cord injured men underestimate their sexual capacity, while diagnoses based on clinical findings are better predictors.

DNase I footprinting experiments showed that binding activities of Sp1 and of GHF-1 to its distal site on the human growth hormone gene promoter are mutually exclusive. The kinetics of GHF-1 binding were indicative of positive cooperativity. The Sp1 site did not affect promoter activity in cell-free transcription. Still, Sp1 could compensate partially for the decreased stimulation of transcription seen at low GHF-1 concentrations.

Transcription of the human growth hormone (hGH) gene and its regulation are controlled by trans-acting factors that bind to hGH gene promoter sequences. Several DNase I footprints have been described within 500 bp of this promoter, one of which (−289 to −267) has not yet been ascribed to a defined factor. By DNase I footprinting, gel mobility shift, and methylation interference assays with extracts from HeLa cells and GH-producing pituitary tumor (GC) cells, we show that this factor belongs to the NF-I family. When NF-I was competed out of the cell extracts, the trans-acting factor AP-2 bound to the same site as NF-I. AP-2 was present not only in HeLa cells, but also in GC cells albeit at a much lower concentration. Consistent with the mutually exclusive binding of NF-I and AP-2, their methylation interference patterns included four guanine residues that were crucial for binding of both NF-I and AP-2. Cell-free transcription from the hGH gene promoter showed that these two factors can transactivate this gene.