Sterile triggers drive joint inflammation in TNF- and IL-1ß-dependent mouse arthritis models.

Arthritis is the most common extra-intestinal complication in inflammatory bowel disease (IBD). Conversely, arthritis patients are at risk for developing IBD and often display subclinical gut inflammation. These observations suggest a shared disease etiology, commonly termed "the gut-joint-axis." The clinical association between gut and joint inflammation is further supported by the success of common therapeutic strategies and microbiota dysbiosis in both conditions. Most data, however, support a correlative relationship between gut and joint inflammation, while causative evidence is lacking. Using two independent transgenic mouse arthritis models, either TNF- or IL-1ß dependent, we demonstrate that arthritis develops independently of the microbiota and intestinal inflammation, since both lines develop full-blown articular inflammation under germ-free conditions. In contrast, TNF-driven gut inflammation is fully rescued in germ-free conditions, indicating that the microbiota is driving TNF-induced gut inflammation. Together, our study demonstrates that although common inflammatory pathways may drive both gut and joint inflammation, the molecular triggers initiating such pathways are distinct in these tissues.

Cell Behavior Changes and Enzymatic Biodegradation of Hybrid Electrospun Poly(3-hydroxybutyrate)-Based Scaffolds with an Enhanced Piezoresponse after the Addition of Reduced Graphene Oxide.

This is the first comprehensive study of the impact of biodegradation on the structure, surface potential, mechanical and piezoelectric properties of poly(3-hydroxybutyrate) (PHB) scaffolds supplemented with reduced graphene oxide (rGO) as well as cell behavior under static and dynamic mechanical conditions. There is no effect of the rGO addition up to 1.0 wt% on the rate of enzymatic biodegradation of PHB scaffolds for 30 d. The biodegradation of scaffolds leads to the depolymerization of the amorphous phase, resulting in an increase in the degree of crystallinity. Because of more regular dipole order in the crystalline phase, surface potential of all fibers increases after the biodegradation, with a maximum (361 ± 5 mV) after the addition of 1 wt% rGO into PHB as compared to pristine PHB fibers. By contrast, PHB-0.7rGO fibers manifest the strongest effective vertical (0.59 ± 0.03 pm V-1 ) and lateral (1.06 ± 0.02 pm V-1 ) piezoresponse owing to a greater presence of electroactive ß-phase. In vitro assays involving primary human fibroblasts reveal equal biocompatibility and faster cell proliferation on PHB-0.7rGO scaffolds compared to pure PHB and nonpiezoelectric polycaprolactone scaffolds. Thus, the developed biodegradable PHB-rGO scaffolds with enhanced piezoresponse are promising for tissue-engineering applications.

Positioning of longest axis of the radial head in neutral forearm rotation.

INTRODUCTION: The radial head has an ellipsoid shape so that a longest and a shortest axis can be defined. The aim of this study is to evaluate the position of the longest axis of the radial head (LARH) in relation to proximal radioulnar joint (PRUJ) and to the forearm in neutral position using 3D computed tomography (CT). MATERIALS AND METHODS: 3D CT reconstructions of the distal humerus, the radius and the ulna of 27 healthy volunteers (average age 27.65 ± 9.25; 24 males, 3 females) were created. First an evaluation of the elliptic form of the radial head and the location of its longest axis was performed. Next, three planes were defined: the PRUJ plane, the forearm plane and a neutral plane. Based on the angle between the forearm plane and the neutral plane, the rotation of the scanned forearm was measured. Taking this rotation into account, the position of the LARH compared to PRUJ plane and forearm plane in neutral position is recalculated. RESULTS: The shape of the radial head is determined to be non-circular based on this study population (p < .001). In neutral position, the angle between the LARH and the forearm plane is 5.28° (SD: 15.09) and between the LARH and the PRUJ is 33.46° (SD: 13.91). CONCLUSIONS: The position of the LARH is found to be approximately perpendicular to the forearm plane when the forearm is in neutral position and perpendicular to the PRUJ plane when the forearm is on average in 30° of pronation.

The influence of cerebrospinal fluid on blood coagulation and the implications for ventriculovenous shunting.

OBJECTIVE: The effect of CSF on blood coagulation is not known. Enhanced coagulation by CSF may be an issue in thrombotic complications of ventriculoatrial and ventriculosinus shunts. This study aimed to assess the effect of CSF on coagulation and its potential effect on thrombotic events affecting ventriculovenous shunts. METHODS: Two complementary experiments were performed. In a static experiment, the effect on coagulation of different CSF mixtures was evaluated using a viscoelastic coagulation monitor. A dynamic experiment confirmed the amount of clot formation on the shunt surface in a roller pump model. RESULTS: CSF concentrations of 9% and higher significantly decreased the activated clotting time (ACT; 164.9 seconds at 0% CSF, 155.6 seconds at 9% CSF, and 145.1 seconds at 32% CSF). Increased clot rates (CRs) were observed starting at a concentration of 5% (29.3 U/min at 0% CSF, 31.6 U/min at 5% CSF, and 35.3 U/min at 32% CSF). The roller pump model showed a significantly greater percentage of shunt surface covered with deposits when the shunts were infused with CSF rather than Ringer's lactate solution (90% vs 63%). The amount of clot formation at the side facing the blood flow (impact side) tended to be lower than that at the side facing away from the blood flow (wake side; 71% vs 86%). CONCLUSIONS: Addition of CSF to blood accelerates coagulation. The CSF-blood-foreign material interaction promotes clot formation, which might result in thrombotic shunt complications. Further development of the ventriculovenous shunt technique should focus on preventing CSF-blood-foreign material interaction and stagnation of CSF in wake zones.