Interfacing External Quantum Devices to a Universal Quantum Computer

We present a scheme to use external quantum devices using the universal quantum computer previously constructed. We thereby show how the universal quantum computer can utilize networked quantum information resources to carry out local computations. Such information may come from specialized quantum devices or even from remote universal quantum computers. We show how to accomplish this by devising universal quantum computer programs that implement well known oracle based quantum algorithms, namely the Deutsch, Deutsch-Jozsa, and the Grover algorithms using external black-box quantum oracle devices. In the process, we demonstrate a method to map existing quantum algorithms onto the universal quantum computer

Disruption of PTH Receptor 1 in T Cells Protects against PTH-Induced Bone Loss

Hyperparathyroidism in humans and continuous parathyroid hormone (cPTH) treatment in mice cause bone loss by regulating the production of RANKL and OPG by stromal cells (SCs) and osteoblasts (OBs). Recently, it has been reported that T cells are required for cPTH to induce bone loss as the binding of the T cell costimulatory molecule CD40L to SC receptor CD40 augments SC sensitivity to cPTH. However it is unknown whether direct PTH stimulation of T cells is required for cPTH to induce bone loss, and whether T cells contribute to the bone catabolic activity of PTH with mechanisms other than induction of CD40 signaling in SCs.Here we show that silencing of PTH receptor 1 (PPR) in T cells blocks the bone loss and the osteoclastic expansion induced by cPTH, thus demonstrating that PPR signaling in T cells is central for PTH-induced reduction of bone mass. Mechanistic studies revealed that PTH activation of the T cell PPR stimulates T cell production of the osteoclastogenic cytokine tumor necrosis factor alpha (TNF). Attesting to the relevance of this effect, disruption of T cell TNF production prevents PTH-induced bone loss. We also show that a novel mechanism by which TNF mediates PTH induced osteoclast formation is upregulation of CD40 expression in SCs, which increases their RANKL/OPG production ratio.These findings demonstrate that PPR signaling in T cells plays an essential role in PTH induced bone loss by promoting T cell production of TNF. A previously unknown effect of TNF is to increase SC expression of CD40, which in turn increases SC osteoclastogenic activity by upregulating their RANKL/OPG production ratio. PPR-dependent stimulation of TNF production by T cells and the resulting TNF regulation of CD40 signaling in SCs are potential new therapeutic targets for the bone loss of hyperparathyroidism

Growth, cell division and sporulation in mycobacteria

Bacteria have the ability to adapt to different growth conditions and to survive in various environments. They have also the capacity to enter into dormant states and some bacteria form spores when exposed to stresses such as starvation and oxygen deprivation. Sporulation has been demonstrated in a number of different bacteria but Mycobacterium spp. have been considered to be non-sporulating bacteria. We recently provided evidence that Mycobacterium marinum and likely also Mycobacterium bovis bacillus Calmette–Guérin can form spores. Mycobacterial spores were detected in old cultures and our findings suggest that sporulation might be an adaptation of lifestyle for mycobacteria under stress. Here we will discuss our current understanding of growth, cell division, and sporulation in mycobacteria

Circulating levels of inflammation and the effect on exercise-related changes in bone mass, structure and strength in middle-aged and older men

Chronic, low-grade systematic inflammation has been associated with bone loss and increased fracture risk. We previously reported that exercise improved femoral neck bone mineral density (BMD), geometry and strength and lumbar spine trabecular BMD in middle-aged and older men, but had no effect on markers of inflammation. The aim of this study was to examine the association between basal inflammatory status and the adaptive skeletal responses to exercise. Secondary analysis was completed on 91 men aged 50–79 years who participated in an 18-month program of progressive resistance training plus weight-bearing impact exercise (3 day/week) with and without additional calcium–vitamin D 3 . Markers of inflammation (serum hs-CRP, TNF-α and IL-6) and DXA and QCT-derived BMD, bone structure and strength at the lumbar spine and proximal femur were measured at baseline and 18 months. Multiple regression was used to assess associations between skeletal changes and both baseline levels of individual inflammatory markers and a composite inflammatory index derived from the number of markers categorized into the highest tertile. Baseline serum hs-CRP, TNFα and IL-6 and the composite inflammatory index score were not associated with skeletal changes at any site after adjusting for age, change in lean mass, disease(s)/medication use and adherence to the exercise intervention. In conclusion, this study indicates that basal inflammatory status does not influence the osteogenic response to exercise training in healthy middle-aged and older men. </p

Usability and effectiveness of Suprathel® in partial thickness burns in children

Trauma Surger