[Elosan therapy : A new treatment option for chronic pain].

Background: The new physical Elosan therapy is designed to provide patients with chronic pain with clear relief, improve their quality of life and reduce the consumption of painkillers. To prove the efficacy and tolerability of this new therapy, a clinical pilot study had to be carried out to certify the Elosan Therapy Cabin as a medical device, since despite extensive literature research no equivalent product or therapy could be identified.

Methodology: In an open, randomized, clinical comparison study at three pain medical centers in Switzerland, a total of 39 patients with chronic pain (duration >6 months; intensity >50 mm visual analog scale (VAS) according to Borg) in two groups (21 verum, 18 control) were included in the study.

Aberrant Proliferation of Differentiating Alveolar Cells Induces Hyperplasia in Resting Mammary Glands of SV40-TAg Transgenic Mice.

WAP-T1 transgenic mice express SV40-TAg under control of the whey acidic protein (WAP) promoter, which directs activity of this strong viral oncogene to luminal cells of the mammary gland. Resting uniparous WAP-T1 glands develop hyperplasia composed of TAg positive cells prior to appearance of advanced tumor stages. We show that cells in hyperplasia display markers of alveolar differentiation, suggesting that TAg targets differentiating cells of the alveolar compartment.

The effects of the "physical BEMER® vascular therapy", a method for the physical stimulation of the vasomotion of precapillary microvessels in case of impaired microcirculation, on sleep, pain and quality of life of patients with different clinical pictures on the basis of three scientifically validated scales.

As part of the statutory market monitoring of certified medical devices, 658 valid patient questionnaires were evaluated between April 2011 and March 2013. The questions consisted mainly of three scientifically recognized scales for assessing the changes of sleep, pain and quality of life in patients who had used the "physical BEMER® vascular therapy" for different diseases over 6 weeks. The result clearly shows that there are significant improvements in all areas surveyed through the application of this complementary treatment option, regardless of the underlying disease.

Silencing of RB1 but not of RB2/P130 induces cellular senescence and impairs the differentiation potential of human mesenchymal stem cells.

Stem cell senescence is considered deleterious because it may impair tissue renewal and function. On the other hand, senescence may arrest the uncontrolled growth of transformed stem cells and protect organisms from cancer. This double function of senescence is strictly linked to the activity of genes that the control cell cycle such as the retinoblastoma proteins RB1, RB2/P130, and P107.

The switch from pRb/p105 to Rb2/p130 in DNA damage and cellular senescence.

Cellular senescence is a response to genotoxic stress that results in an irreversible cell cycle arrest. Activation of this pathway relies on the activity of the retinoblastoma proteins and proteins of the DNA damage response cascade. Here, we discuss the functional relevance of the switch from pRb/p105 to Rb2/p130 that becomes apparent when cells enter senescent arrest.

Nestin modulates glucocorticoid receptor function by cytoplasmic anchoring.

Nestin is the characteristic intermediate filament (IF) protein of rapidly proliferating progenitor cells and regenerating tissue. Nestin copolymerizes with class III IF-proteins, mostly vimentin, into heteromeric filaments. Its expression is downregulated with differentiation.

In vitro senescence of rat mesenchymal stem cells is accompanied by downregulation of stemness-related and DNA damage repair genes.

Mesenchymal stem cells (MSCs) are of particular interest because they are being tested using cell and gene therapies for a number of human diseases. MSCs represent a rare population in tissues. Therefore, it is essential to grow MSCs in vitro before putting them into therapeutic use.

Activation of the glucocorticoid receptor releases unstimulated PBMCs from an early block in HIV-1 replication.

Infection of resting peripheral mononuclear blood cells (PBMCs) with HIV-1 is not productive due to a block prior to integration of the provirus into the host genome. Here we show that a unique restriction is determined by the status of the glucocorticoid receptor (GR). Proviral integration increases after addition of a GR ligand.

Cytoplasmic localization of wild-type p53 in glioblastomas correlates with expression of vimentin and glial fibrillary acidic protein.

Cytoplasmic accumulation of wild-type p53 in tumor cells indicates that the tumor suppressor is inactive with regard to growth suppressive functions. Whether this occurs randomly during tumor development or characterizes a certain tumor cell subset is not known. Here we assayed primary glioblastomas for expression and subcellular localization of p53 and determined a correlation with expression of intermediate filament proteins characterizing glial cell development.