New thermocouple-based microwave/millimeter-wave power sensor MMIC techniques in GaAs

We describe a new RF and microwave power sensor monolithic microwave integrated circuit design. The circuit incorporates a number of advances over existing designs. These include a III–V epitaxial structure optimized for sensitivity, the figure-of-merit applicable to the optimization, a mechanism for in-built detection of load ageing and damage to extend calibration intervals, and a novel symmetrical structure to linearize the high-power end of the scale

The Masses of Transition Circumstellar Disks: Observational Support for Photoevaporation Models

We report deep Sub-Millimeter Array observations of 26 pre-main-sequence (PMS) stars with evolved inner disks. These observations measure the mass of the outer disk (r ~20-100 AU) across every stage of the dissipation of the inner disk (r < 10 AU) as determined by the IR spectral energy distributions (SEDs). We find that only targets with high mid-IR excesses are detected and have disk masses in the 1-5 M_Jup range, while most of our objects remain undetected to sensitivity levels of M_DISK ~0.2-1.5 M_Jup. To put these results in a more general context, we collected publicly available data to construct the optical to millimeter wavelength SEDs of over 120 additional PMS stars. We find that the near-IR and mid-IR emission remain optically thick in objects whose disk masses span 2 orders of magnitude (~0.5-50 M_Jup). Taken together, these results imply that, in general, inner disks start to dissipate only after the outer disk has been significantly depleted of mass. This provides strong support for photoevaporation being one of the dominant processes driving disk evolution.Comment: Accepted for publication by ApJL, 4 pages and 3 figure

The experiences of ethnic minority MSM with NHS sexual health services in Britain

Objective: To compare the experiences of ethnic minority and white British men who have sex with men (MSM) who attend National Health Service (NHS) sexual health clinics in Britain. Methods: In 2007-2008 a national sample of MSM living in Britain was recruited through websites, in sexual health clinics, bars, clubs and other venues. Men completed an online survey which included questions about their experience of attending an NHS sexual health clinic. Results: Analysis is restricted to 363 ethnic minority MSM and 4776 white British MSM who had attended an NHS sexual health clinic in the 12 months before the survey. Compared with white British men, men from an Indian, Pakistani or Bangladeshi background were more likely to be very anxious about attending the clinic (adjusted odds ratio (aOR) 2.58, 95% confidence interval (CI) 1.63, 4.07), express concerns about being overheard at reception (aOR 1.68, 95% CI 1.10, 2.58), be uncomfortable in the waiting area (aOR 2.04, 95% CI 1.32, 3.15), or be afraid that people in their community would find out that they have sex with men (aOR 7.70, 95% CI 4.49,13.22). The adjusted odds ratios for being afraid that people in their community would find out that they have sex with men were also elevated for black Caribbean, black African, Chinese and other Asian men. Conclusion: Sexual health clinics should be aware that some ethnic minority MSM, particularly those from an Indian, Pakistani or Bangladeshi background, have heightened concerns about clinic attendance and confidentiality compared with white British MSM

Brainstem Raphe Pallidus and the Adjacent Area Contain a Novel Action Site in the Melanocortin Circuitry Regulating Energy Balance

The central melanocortin system plays a critical role in the regulation of energy balance in rodents and humans. The melanocortin signals in both the hypothalamus and brainstem contribute to this regulation. However, how the melanocortin signals of the hypothalamus interact with those intrinsic to the brainstem in the regulation of energy balance is poorly understood. The brainstem raphe pallidus (RPa) and adjacent areas contain melanocortin 4 receptor (MC4-R)-bearing neurons and sympathetic premotor neurons regulating thermogenesis. Here we report that α-melanocyte-stimulating hormone (α-MSH)-immunoreactive (IR) fibers are in close apposition to MC4-R neurons in the RPa. Retrograde tracing studies revealed a unique direct projection from hypothalamic proopiomelanocortin (POMC) neurons to the RPa and adjacent areas of the brainstem in mice and rats. Furthermore, microinjection of the MC3/4-R agonist MTII into the RPa area dose-dependently stimulated oxygen consumption and inhibited feeding, whereas microinjection of the antagonist, SHU9119, enhanced feeding. These data suggest a novel pathway of hypothalamic POMC neuronal efferents to brainstem RPa area MC4-R neurons in the melanocortin circuitry that contribute to coordinate regulation of energy balance

Protostellar Outflow Evolution in Turbulent Environments

The link between turbulence in star formatting environments and protostellar jets remains controversial. To explore issues of turbulence and fossil cavities driven by young stellar outflows we present a series of numerical simulations tracking the evolution of transient protostellar jets driven into a turbulent medium. Our simulations show both the effect of turbulence on outflow structures and, conversely, the effect of outflows on the ambient turbulence. We demonstrate how turbulence will lead to strong modifications in jet morphology. More importantly, we demonstrate that individual transient outflows have the capacity to re-energize decaying turbulence. Our simulations support a scenario in which the directed energy/momentum associated with cavities is randomized as the cavities are disrupted by dynamical instabilities seeded by the ambient turbulence. Consideration of the energy power spectra of the simulations reveals that the disruption of the cavities powers an energy cascade consistent with Burgers'-type turbulence and produces a driving scale-length associated with the cavity propagation length. We conclude that fossil cavities interacting either with a turbulent medium or with other cavities have the capacity to sustain or create turbulent flows in star forming environments. In the last section we contrast our work and its conclusions with previous studies which claim that jets can not be the source of turbulence.Comment: 24 pages, submitted to the Astrophysical Journa

Dysfunctional stem and progenitor cells impair fracture healing with age

Successful fracture healing requires the simultaneous regeneration of both the bone and vasculature; mesenchymal stem cells (MSCs) are directed to replace the bone tissue, while endothelial progenitor cells (EPCs) form the new vasculature that supplies blood to the fracture site. In the elderly, the healing process is slowed, partly due to decreased regenerative function of these stem and progenitor cells. MSCs from older individuals are impaired with regard to cell number, proliferative capacity, ability to migrate, and osteochondrogenic differentiation potential. The proliferation, migration and function of EPCs are also compromised with advanced age. Although the reasons for cellular dysfunction with age are complex and multidimensional, reduced expression of growth factors, accumulation of oxidative damage from reactive oxygen species, and altered signaling of the Sirtuin-1 pathway are contributing factors to aging at the cellular level of both MSCs and EPCs. Because of these geriatric-specific issues, effective treatment for fracture repair may require new therapeutic techniques to restore cellular function. Some suggested directions for potential treatments include cellular therapies, pharmacological agents, treatments targeting age-related molecular mechanisms, and physical therapeutics. Advanced age is the primary risk factor for a fracture, due to the low bone mass and inferior bone quality associated with aging; a better understanding of the dysfunctional behavior of the aging cell will provide a foundation for new treatments to decrease healing time and reduce the development of complications during the extended recovery from fracture healing in the elderly

Isotropically Driven versus Outflow Driven Turbulence: Observational Consequences for Molecular Clouds

Feedback from protostellar outflows can influence the nature of turbulence in star forming regions even if they are not the primary source of velocity dispersion for all scales of molecular clouds. For the rate and power expected in star forming regions, we previously (Carroll et al. 2009) demonstrated that outflows could drive supersonic turbulence at levels consistent with the scaling relations from Matzner 2007 although with a steeper velocity power spectrum than expected for an isotropically driven supersonic turbulent cascade. Here we perform higher resolution simulations and combine simulations of outflow driven turbulence with those of isotropically forced turbulence. We find that the presence of outflows within an ambient isotropically driven turbulent environment produces a knee in the velocity power spectrum at the outflow scale and a steeper slope at sub-outflow scales than for a purely isotropically forced case. We also find that the presence of outflows flattens the density spectrum at large scales effectively reducing the formation of large scale turbulent density structures. These effects are qualitatively independent of resolution. We have also carried out Principal Component Analysis (PCA) for synthetic data from our simulations. We find that PCA as a tool for identifying the driving scale of turbulence has a misleading bias toward low amplitude large scale velocity structures even when they are not necessarily the dominant energy containing scales. This bias is absent for isotropically forced turbulence but manifests strongly for collimated outflow driven turbulence.Comment: 30 pages, 10 figures, Submitted to Ap

Contribution of Endogenous Glucocorticoids and Their Intravascular Metabolism by 11β-HSDs to Postangioplasty Neointimal Proliferation in Mice

Exogenous glucocorticoids inhibit neointimal proliferation in animals. We aime to test the hypothesis that endogenous glucocorticoids influence neointimal proliferation; this may be mediated by effects on systemic risk factors or locally in vessels, and modulated either by adrenal secretion or by enzymes expressed in vessels which mediate local inactivation (11β-HSD2 in endothelium) or regeneration (11β-HSD1 in smooth muscle) of glucocorticoids. Femoral artery wire-angioplasty was conducted in C57Bl/6J, Apo-E(−/−), 11β-HSD1(−/−), Apo-E, 11β-HSD1(−/−) (double knockout) and 11β-HSD2(−/−) mice following glucocorticoid administration, adrenalectomy, glucocorticoid or mineralocorticoid receptor antagonism, or selective 11β-HSD1 inhibition. In C57Bl/6J mice, neointimal proliferation was reduced by systemic or local glucocorticoid administration, unaffected by adrenalectomy, reduced by the mineralocorticoid receptor antagonist eplerenone, and increased by the glucocorticoid receptor antagonist RU38486. 11β-HSD2 deletion had no effect on neointimal proliferation, with or without eplerenone. 11β-HSD1 inhibition or deletion had no effect in chow-fed C57Bl/6J mice, but reduced neointimal proliferation in Apo-E(−/−) mice on Western diet. Reductions in neointimal size were accompanied by reduced macrophage and increased collagen content. We conclude that pharmacological administration of glucocorticoid receptor agonists or of mineralocorticoid receptor antagonists may be useful in reducing neointimal proliferation. Endogenous corticosteroids induce beneficial glucocorticoid receptor activation and adverse mineralocorticoid receptor activation. However, manipulation of glucocorticoid metabolism has beneficial effects only in mice with exaggerated systemic risk factors, suggesting effects mediated primarily in liver and adipose rather than intra-vascular glucocorticoid signalling. Reducing glucocorticoid action with 11β-HSD1 inhibitors that are being developed for type 2 diabetes appears not to risk enhanced neointimal proliferation

Hypertension in mice lacking 11beta-hydroxysteroid dehydrogenase type 2

Deficiency of 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) in humans leads to the syndrome of apparent mineralocorticoid excess (SAME), in which cortisol illicitly occupies mineralocorticoid receptors, causing sodium retention, hypokalemia, and hypertension. However, the disorder is usually incompletely corrected by suppression of cortisol, suggesting additional and irreversible changes, perhaps in the kidney. To examine this further, we produced mice with targeted disruption of the 11β-HSD2 gene. Homozygous mutant mice (11β-HSD2(–/–)) appear normal at birth, but ∼50% show motor weakness and die within 48 hours. Both male and female survivors are fertile but exhibit hypokalemia, hypotonic polyuria, and apparent mineralocorticoid activity of corticosterone. Young adult 11β-HSD2(–/–) mice are markedly hypertensive, with a mean arterial blood pressure of 146 ± 2 mmHg, compared with 121 ± 2 mmHg in wild-type controls and 114 ± 4 mmHg in heterozygotes. The epithelium of the distal tubule of the nephron shows striking hypertrophy and hyperplasia. These histological changes do not readily reverse with mineralocorticoid receptor antagonism in adulthood. Thus, 11β-HSD2(–/–) mice demonstrate the major features of SAME, providing a unique rodent model to study the molecular mechanisms of kidney resetting leading to hypertension. J. Clin. Invest. 103:683–689 (1999