Measurement of active shoulder proprioception: dedicated system and device

Proprioception is an essential part of shoulder stability and neuromuscular control. The purpose of the study was the development of a precise system of shoulder proprioception assessment in the active mode (Propriometr). For that purpose, devices such as the electronic goniometer and computer software had been designed. A pilot study was carried out on a control group of 27 healthy subjects, the average age being 23.8 (22–29) in order to test the system. The result of the assessment was the finding of the error of active reproduction of the joint position (EARJP). EARJP was assessed for flexion, abduction, external and internal rotation. For every motion, reference positions were used at three different angles. The results showed EARJP to range in 3–6.1°. The proprioception evaluation system (propriometr) allows a precise measurement of active joint position sense. The designed system can be used to assess proprioception in both shoulder injuries and treatment. In addition, all achieved results of normal shoulders may serve as reference to be compared with the results of forthcoming studies.     

The spread of medical fake news in social media – The pilot quantitative study

Objectives

Fake news: misinformation and falsehood of health news in social media constitute a potential threat to the public health, but the scope of this issue remains unclear. Our pilot study is an initial attempt to measure a number of the top shared health misinformation stories in the Polish language social media.

Effect of Co Substitution and Thermo-Magnetic Treatment on the Structure and Induced Magnetic Anisotropy of Fe84.5−xCoxNb5B8.5P2 Nanocrystalline Alloys

In the present work, we investigated in detail the thermal/crystallization behavior and magnetic properties of materials with Fe_84.5-xCo_xNb₅B_8.5P₂ (x = 0, 5, 10, 15 and 20 at.%) composition. The amorphous ribbons were manufactured on a semi-industrial scale by the melt-spinning technique. The subsequent nanocrystallization processes were carried out under different conditions (with/without magnetic field). The comprehensive studies have been carried out using differential scanning calorimetry, X-ray diffractometry, transmission electron microscopy, hysteresis loop analyses, vibrating sample magnetometry and Mössbauer spectroscopy. Moreover, the frequency (up to 300 kHz) dependence of power losses and permeability at a magnetic induction up to 0.9 T was investigated. On the basis of some of the results obtained, we calculated the values of the activation energies and the induced magnetic anisotropies. The X-ray diffraction results confirm the surface crystallization effect previously observed for phosphorous-containing alloys. The in situ microscopic observations of crystallization describe this process in detail in accordance with the calorimetry results. Furthermore, the effect of Co content on the phase composition and the influence of annealing in an external magnetic field on magnetic properties, including the orientation of the magnetic spins, have been studied using various magnetic techniques. Finally, nanocrystalline Fe_64.5Co₂₀Nb₅B_8.5P₂ cores were prepared after transverse thermo-magnetic heat treatment and installed in industrially available portable heating equipment.     

Biological and Pro-Angiogenic Properties of Genetically Modified Human Primary Myoblasts Overexpressing Placental Growth Factor in In Vitro and In Vivo Studies

Cardiovascular diseases are a growing problem in developing countries; therefore, there is an ongoing intensive search for new approaches to treat these disorders. Currently, cellular therapies are focused on healing the damaged heart by implanting stem cells modified with pro-angiogenic factors. This approach ensures that the introduced cells are capable of fulfilling the complex requirements of the environment, including the replacement of the post-infarction scar with cells that are able to contract and promote the formation of new blood vessels that can supply the ischaemic region with nutrients and oxygen. This study focused on the genetic modification of human skeletal muscle cells (SkMCs). We chose myoblast cells due to their close biological resemblance to cardiomyocytes and the placental growth factor (PlGF) gene due to its pro-angiogenic potential. In our in vitro studies, we transfected SkMCs with the PlGF gene using electroporation, which has previously been proven to be efficient and generate robust overexpression of the PlGF gene and elevate PlGF protein secretion. Moreover, the functionality of the secreted pro-angiogenic proteins was confirmed using an in vitro capillary development assay. We have also examined the influence of PlGF overexpression on VEGF-A and VEGF-B, which are well-known factors described in the literature as the most potent activators of blood vessel formation. We were able to confirm the overexpression of VEGF-A in myoblasts transfected with the PlGF gene. The results obtained in this study were further verified in an animal model. These data were able to confirm the potential therapeutic effects of the applied treatments.

     

Heterozygous CTNNB1 and TBX4 variants in a patient with abnormal lung growth,pulmonary hypertension,microcephaly, and spasticity

The canonical wingless (Wnt) and fibroblast growth factor (FGF) signaling pathways involving CTNNB1 and TBX4, respectively, are crucial for the regulation of human development. Perturbations of these pathways and disruptions from biological homeostasis have been associated with abnormal morphogenesis of multiple organs, including the lung. The aim of this study was to identify the underlying genetic cause of abnormal lung growth, pulmonary hypertension (PAH), severe microcephaly, and muscle spasticity in a full-term newborn, who died at 4 months of age due to progressively worsening PAH and respiratory failure. Family trio exome sequencing showed a de novo heterozygous nonsense c.1603C>T (p.Arg535*) variant in CTNNB1 and a paternally inherited heterozygous missense c.1198G>A (p.Glu400Lys) variant in TBX4, both predicted to be likely deleterious. We expand the phenotypic spectrum associated with CTNNB1 and TBX4 variants and indicate that they could act synergistically to produce a distinct more severe phenotype. Our findings further support a recently proposed complex compound inheritance model in lethal lung developmental diseases and the contention that dual molecular diagnoses can parsimoniously explain blended phenotypes.     

Infarct volume varies with rat strain and vendor in focal cerebral ischemia induced by transcranial middle cerebral artery occlusion

We recently reported that the outcome of focal cerebral ischemia induced by intraluminal middle cerebral artery occlusion may differ depending upon a rat's strain and/or vendor. Sprague-Dawley rats originating from Taconic Laboratories and Charles River Laboratories had infarct volumes several fold larger than Sprague-Dawley rats originating from Simonsen Laboratories. The present study sought to determine whether these differences were restricted to an intraluminal technique or whether strain and vendor dependent differences will also exist in rats subjected to a transcranial method of focal cerebral ischemia. Accordingly, we permanently coagulated the middle cerebral artery via a transcranial approach in Sprague-Dawley rats originating from Simonsen Laboratories and Taconic Laboratories and in Simonsen Laboratories Fischer-344 rats. The cortical infarct volume significantly differed in the following order: Simonsen Laboratories Sprague-Dawley rats < Simonsen Laboratories Fischer-344 rats < Taconic Laboratories Sprague-Dawley rats. The subcortical infarct volume differed statistically in the following order: Simonsen Laboratories Sprague-Dawley rats < Taconic Laboratories Sprague-Dawley rats < Simonsen Laboratories Fischer-344 rats. These results along with our previous findings demonstrate that strain and vendor differences in the outcome of focal cerebral ischemia are independent of the technique applied.     

Neuronal sirtuin1 mediates retinal vascular regeneration in oxygen-induced ischemic retinopathy

Regeneration of blood vessels in ischemic neuronal tissue is critical to reduce tissue damage in diseases. In proliferative retinopathy, initial vessel loss leads to retinal ischemia, which can induce either regrowth of vessels to restore normal metabolism and minimize damage, or progress to hypoxia-induced sight-threatening pathologic vaso-proliferation. It is not well understood how retinal neurons mediate regeneration of vascular growth in response to ischemic insults. In this study we aim to investigate the potential role of Sirtuin 1 (Sirt1), a metabolically-regulated protein deacetylase, in mediating the response of ischemic neurons to regulate vascular regrowth in a mouse model of oxygen-induced ischemic retinopathy (OIR). We found that Sirt1 is highly induced in the avascular ischemic retina in OIR. Conditional depletion of neuronal Sirt1 leads to significantly decreased retinal vascular regeneration into the avascular zone and increased hypoxia-induced pathologic vascular growth. This effect is likely independent of PGC-1α, a known Sirt1 target, as absence of PGC-1α in knockout mice does not impact vascular growth in retinopathy. We found that neuronal Sirt1 controls vascular regrowth in part through modulating deacetylation and stability of hypoxia-induced factor 1α and 2α, and thereby modulating expression of angiogenic factors. These results indicate that ischemic neurons induce Sirt1 to promote revascularization into ischemic neuronal areas, suggesting a novel role of neuronal Sirt1 in mediating vascular regeneration in ischemic conditions, with potential implications beyond retinopathy.     

Evidence that orexins A and B stimulate insulin secretion from rat pancreatic islets via both receptor subtypes

Orexins are recently identified neuropeptides that appear to play a role in the regulation of energy homeostasis and arousal. They bind to and activate two closely related G protein-coupled receptors (OXR1 and OXR2), previously described as orphans. In this study we examined involvement of orexins in regulation of insulin secretion from rat pancreatic islets utilizing an in situ perfused pancreas and isolated pancreatic islet models. By means of RT-PCR we found that both OXR1 and OXR2 are expressed in rat pancreatic islets. Furthermore, the expression levels of OXR1 were higher than OXR2. In both experimental models applied, orexins A and B (1, 10 and 100 nmol/l) concentration dependently stimulated insulin secretion at two different glucose concentrations (6.66 or 26.4 mmol/l), with orexin A being more potent than orexin B. This study demonstrates that orexins A and B modulate insulin secretion in vitro.     

Basolateral junctions are sufficient to suppress epithelial invasion during Drosophila oogenesis.

Epithelial junctions play crucial roles during metazoan evolution and development by facilitating tissue formation, maintenance, and function. Little is known about the role of distinct types of junctions in controlling epithelial transformations leading to invasion of neighboring tissues. Discovering the key junction complexes that control these processes and how they function may also provide mechanistic insight into carcinoma cell invasion. Here, using the Drosophila ovary as a model, we show that four proteins of the basolateral junction (BLJ), Fasciclin-2, Neuroglian, Discs-large, and Lethal-giant-larvae, but not proteins of other epithelial junctions, directly suppress epithelial tumorigenesis and invasion. Remarkably, the expression pattern of Fasciclin-2 predicts which cells will invade. We compared the apicobasal polarity of BLJ tumor cells to border cells (BCs), an epithelium-derived cluster that normally migrates during mid-oogenesis. Both tumor cells and BCs differentiate a lateralized membrane pattern that is necessary but not sufficient for invasion. Independent of lateralization, derepression of motility pathways is also necessary, as indicated by a strong linear correlation between faster BC migration and an increased incidence of tumor invasion. However, without membrane lateralization, derepression of motility pathways is also not sufficient for invasion. Our results demonstrate that spatiotemporal patterns of basolateral junction activity directly suppress epithelial invasion by organizing the cooperative activity of distinct polarity and motility pathways.     

No contribution of multipotent mesenchymal stromal cells to liver regeneration in a rat model of prolonged hepatic injury

Multipotent mesenchymal stromal (MS) cells from adult bone marrow are a cell population that can be expanded to large numbers in culture. MS cells might be differentiated toward hepatocytes in vitro and thus are promising candidates for therapeutic applications in vivo. The efficacy of bone marrow-derived MS cells versus hepatocytes to contribute to liver regeneration was compared in a rat model of prolonged toxic hepatic injury. Liver damage was induced by injection of carbon tetrachloride (CCl(4)) or allyl alcohol (AA) with and without retrorsine (R) pretreatment. MS cells or hepatocytes of wild-type F344 rats were injected into dipeptidyl peptidase IV (DPPIV)-deficient syngeneic rats. Hepatocyte chimerism was higher after intraportal hepatocyte transplantation in the R/AA group (mean maximal cluster size [MCS] = 21 cells) compared with the R/CCl(4) treatment group (MCS = 18). No hepatocyte engraftment was outlined following post-transplant CCl(4) injection only, whereas mere AA injection resulted in small clusters of donor-derived hepatocytes (MCS = 2). Intraparenchymal injection of hepatocytes was associated with a MCS = 11 after R/AA treatment and a MCS = 6 after AA administration alone. Redistribution of MS cells to the liver was shown after intraportal and intraparenchymal injection. In contrast to hepatocyte transplantation, however, donor-derived DPPIV-positive cells could not be demonstrated in any recipient after MS cell transplantation. Data from the present study indicate that a well-defined population of MS cells obtained according to established standard protocols does not differentiate into hepatocytes in vivo when transplanted under regenerative conditions, in which the application of hepatocytes results in stable hepatic engraftment.