Nonlinear Generation of Electromagnetic Waves through Induced Scattering by Thermal Plasma.

We demonstrate the conversion of electrostatic pump waves into electromagnetic waves through nonlinear induced scattering by thermal particles in a laboratory plasma. Electrostatic waves in the whistler branch are launched that propagate near the resonance cone. When the amplitude exceeds a threshold ~5 × 10(-6) times the background magnetic field, wave power is scattered below the pump frequency with wave normal angles (~59°), where the scattered wavelength reaches the limits of the plasma column. The scattered wave has a perpendicular wavelength that is an order of magnitude larger than the pump wave and longer than the electron skin depth. The amplitude threshold, scattered frequency spectrum, and scattered wave normal angles are in good agreement with theory. The results may affect the analysis and interpretation of space observations and lead to a comprehensive understanding of the nature of the Earth's plasma environment.

Spontaneous electromagnetic emission from a strongly localized plasma flow.

Laboratory observations of electromagnetic ion-cyclotron waves generated by a localized transverse dc electric field are reported. Experiments indicate that these waves result from a strong E×B flow inhomogeneity in a mildly collisional plasma with subcritical magnetic field-aligned current. The wave amplitude scales with the magnitude of the applied radial dc electric field. The electromagnetic signatures become stronger with increasing plasma ß, and the radial extent of the power is larger than that of the electrostatic counterpart. Near-Earth space weather implications of the results are discussed.

Head and neck squamous cell carcinoma transcriptome analysis by comprehensive validated differential display.

Head and neck squamous cell carcinoma (HNSCC) is common worldwide and is associated with a poor rate of survival. Identification of new markers and therapeutic targets, and understanding the complex transformation process, will require a comprehensive description of genome expression, that can only be achieved by combining different methodologies. We report here the HNSCC transcriptome that was determined by exhaustive differential display (DD) analysis coupled with validation by different methods on the same patient samples. The resulting 820 nonredundant sequences were analysed by high throughput bioinformatics analysis. Human proteins were identified for 73% (596) of the DD sequences. A large proportion (>50%) of the remaining unassigned sequences match ESTs (expressed sequence tags) from human tumours. For the functionally annotated proteins, there is significant enrichment for relevant biological processes, including cell motility, protein biosynthesis, stress and immune responses, cell death, cell cycle, cell proliferation and/or maintenance and transport. Three of the novel proteins (TMEM16A, PHLDB2 and ARHGAP21) were analysed further to show that they have the potential to be developed as therapeutic targets.

The role of lower-hybrid-wave collapse in the auroral ionosphere.

In regions where lower-hybrid solitary structures (LHSS) are observed, the character of auroral lower-hybrid turbulence (LHT) (0-20 kHz) is investigated using the amplitude probability distribution of the electric field. The observed probability distributions are accurately described by a Rayleigh distribution with two degrees of freedom. The statistics of the LHT exhibit no evidence of the global modulational instability or self-similar wave collapse. We conclude that nucleation and resonant scattering in preexisting density depletions are the processes responsible for LHSS in auroral LHT.

Effect of trapped ions on shielding of a charged spherical object in a plasma.

Collisions have traditionally been neglected in calculating the shielding around a small spherical collector in a plasma, and the plasma flow to the collector. We show analytically that, in dusty plasmas under typical discharge conditions, ion charge-exchange collisions lead to the buildup of negative-energy trapped ions which dominate the shielding cloud in the nonlinear region near a dust grain and substantially increase the ion current to the grain, even when the mean-free path is much greater than the Debye length.

MDM2 induces hyperplasia and premalignant lesions when expressed in the basal layer of the epidermis.

The MDM2 oncogene is overexpressed in 5-10% of human tumours. Its major physiological role is to inhibit the tumour suppressor p53. However, MDM2 has p53-independent effects on differentiation and does not predispose to tumorigenesis when it is expressed in the granular layer of the epidermis. These unexpected properties of MDM2 could be tissue specific or could depend on the differentiation state of the cells. Strikingly, we found that MDM2 has p53-dependent effects on differentiation, proliferation and apoptosis when it is expressed in the less differentiated basal layer cells. MDM2 inhibits UV induction of p53, the cell cycle inhibitor p21(WAF1/CIP1) and apoptosis ('sunburn cells'). Importantly, MDM2 increases papilloma formation induced by chemical carcinogenesis and predisposes to the appearance of premalignant lesions and squamous cell carcinomas. p53 has a natural role in the protection against UV damage in the basal layer of the epidermis. Our results show that MDM2 predisposes to tumorigenesis when expressed at an early stage of differentiation, and provide a mouse model of MDM2 tumorigenesis relevant to p53's tumour suppressor functions.

MDM2 overexpression generates a skin phenotype in both wild type and p53 null mice.

The MDM2 proto-oncogene is overexpressed in human tumours and regulates the activities of the tumour suppressors p53 and pRB. We created mice that overexpress MDM2 under the control of the CMV promoter. These mice did not display an increased tumour incidence, but rather a specific skin phenotype, characterized by desquamation and hyperkeratosis. Transgenic MDM2 was found to be overexpressed in the epidermis, a tissue that normally expresses high levels of MDM2. The phenotype appeared during the first week after birth and then lessened with age, closely following the level of expression of the transgene. MDM2 overexpression was associated with an increase in proliferation in the basal layer, thickening of the epidermis, altered expression of the differentiation markers cytokeratin CK14, CK10 and CK1, and a decrease in the size and the number of granules that contain products of differentiation. Transgenic mice on a p53 null background displayed similar although not identical changes, showing that the effects of MDM2 are to a certain degree p53 independent. The skin is a major site of MDM2 expression in mice, raising the possibility that MDM2 overexpression perturbs the normal pattern of MDM2 expression and inhibits differentiation of the epidermis.

Fibrinolysis in idiopathic menorrhagia.

Serum fibrin/fibrinogen degradation product (FDP) was studied in 64 patients of menorrhagia without any organic cause in addition to 24 healthy women by Thrombo - Wellcotest HA - 13 Kit (Wellcome, England). Serum FDP levels were found to be less than 10 micrograms/ml in healthy subjects, whereas in idiopathic menorrhagia it was more than 10 micrograms/ml in 59.34% patients. Semi-quantitative estimation of FDP in 14 patients of idiopathic menorrhagia indicated a positive correlation between duration of bleeding and FDP levels. Bleeding appears to be due to increased fibrinolytic activity in uterus secondary to plasminogen activator. Such patients are likely to be benefitted with anti-fibrinolytic agents.

Auditing medical records helps reduce liability.

An internal audit of a hospital's medical records department compares the department to standards developed by the hospital and to benchmarks set by accrediting organizations. An auditor can review the department's economy and effectiveness through employee surveys, direct observation, and interviews. By uncovering deficiencies and making recommendations for their correction, an internal audit can help limit a hospital's liability exposure.