The small world coefficient 4.8 ± 1 optimizes information processing in 2D neuronal networks.

Small world networks have recently attracted much attention because of their unique properties. Mounting evidence suggests that communication is optimized in networks with a small world topology. However, despite the relevance of the argument, little is known about the effective enhancement of information in similar graphs. Here, we provide a quantitative estimate of the efficiency of small world networks. We used a model of the brain in which neurons are described as agents that integrate the signals from other neurons and generate an output that spreads in the system. We then used the Shannon Information Entropy to decode those signals and compute the information transported in the grid as a function of its small-world-ness ([Formula: see text]), of the length ([Formula: see text]) and frequency ([Formula: see text]) of the originating stimulus. In numerical simulations in which [Formula: see text] was varied between [Formula: see text] and [Formula: see text] we found that, for certain values of [Formula: see text] and [Formula: see text], communication is enhanced up to [Formula: see text] times compared to unstructured systems of the same size. Moreover, we found that the information processing capacity of a system steadily increases with [Formula: see text] until the value [Formula: see text], independently on [Formula: see text] and [Formula: see text]. After this threshold, the performance degrades with [Formula: see text] and there is no convenience in increasing indefinitely the number of active links in the system. Supported by the findings of the work and in analogy with the exergy in thermodynamics, we introduce the concept of exordic systems: a system is exordic if it is topologically biased to transmit information efficiently.

New frontiers and emerging applications of 3D printing in ENT surgery: a systematic review of the literature.

3D printing systems have revolutionised prototyping in the industrial field by lowering production time from days to hours and costs from thousands to just a few dollars. Today, 3D printers are no more confined to prototyping, but are increasingly employed in medical disciplines with fascinating results, even in many aspects of otorhinolaryngology. All publications on ENT surgery, sourced through updated electronic databases (PubMed, MEDLINE, EMBASE) and published up to March 2017, were examined according to PRISMA guidelines. Overall, 121 studies fulfilled specific inclusion criteria and were included in our systematic review. Studies were classified according to the specific field of application (otologic, rhinologic, head and neck) and area of interest (surgical and preclinical education, customised surgical planning, tissue engineering and implantable prosthesis). Technological aspects, clinical implications and limits of 3D printing processes are discussed focusing on current benefits and future perspectives.

Degradation of hyaluronic acid by photosensitized riboflavin in vitro. Modulation of the effect by transition metals, radical quenchers, and metal chelators.

The effect of photoexcited riboflavin (RF) on the viscosity of hyaluronic acid (HA) solutions has been investigated. UV irradiation of RF causes under aerobic conditions fragmentation of HA and a decrease in the viscosity of its solutions. A decrease of HA viscosity occurs in PO(4)-buffered solutions and is accelerated by high pH, Fe2+ (but much less so by Fe3+), certain metal chelators, and horseradish peroxidase (HRP); it is partially inhibited by catalase and less so by superoxide dismutase (SOD). The reactivity of the system was completely blocked by Tris, ethanol, aspirin, d-manitol, dimethylthiourea (DMTU), dimethylsulfoxide (DMSO), and sodium azide. These results indicate that the most likely chemical species involved in the reaction is the hydroxyl radical. Singlet oxygen ((1)O(2)) generation is suggested by the ability of NaN3 and DMSO to completely inhibit the reactivity of the system. These two agents, however, may also interact with OH. radical, as well and suppress the reactivity of the system. H(2)O(2) and O(2).- seem also to be produced in significant amounts, because catalase and SOD partially block the reactivity of the system. The effect of HRP may be due to hydrogen subtraction from HA and H(2)O(2) reduction to water. Photoexcitation of RF may potentially occur in vitro and in vivo in the organs and tissues that are permeable to light, such as the eye or skin, and damage HA and other cell-matrix components causing inflammation and accelerating aging.

[Effect of oxaceprol on the structure of proteoglycans synthesized by articular chondrocytes from calves]. / Effet de l'oxacéprol sur la structure des protéoglycannes synthétisés par les chondrocytes articulaires de veau.

Calf articular cartilage fragments were incubated in vitro in the absence and presence of 170 micrograms N-acethyl-trans-4, hydroxyproline (oxaceprol) and 20 muCi [35S]-Na2SO4 per ml of culture medium. Newly synthesized 35S labeled proteoglycans (35S-PGs) were extracted with buffered 4M guanidinium chloride (GdmCl) solvent and then characterized with respect to their hydrodynamic sizes, capacity to interact and form aggregates with hyaluronic acid (AH) and the length and composition of their glycosaminoglycan (GAG) side chains. It was demonstrated that extracted 35S-PGs synthesized in the presence of the oxaceprol are not significantly different from the molecules synthesized in the absence of this compound.

[Effect of oxaceprol on the synthesis and degradation in vitro of proteoglycans and proteins by calf articular cartilage explants]. / Effet de l'oxacéprol sur la synthèse et la dégradation in vitro des protéoglycannes et des protéines par des explants de cartilage articulaire de veau.

The authors have studied in organ culture, the effects of oxaceprol-structural analogue of hydroxyproline, on the proteoglycan and protein synthesis and degradation by calf articular chondrocytes. A stimulation of the incorporation of 35SO4, which indicate proteoglycan synthesis, was shown. The effect was observed at concentrations 10(-6) M to 10(-9) M, i.e. at 170 ng to 170 pg of the oxaceprol per ml of culture media, respectively. However, no significant effect was seen at concentrations 10(-4) M (17 micrograms/ml) to 10(-8) M (1.7 ng/ml) on the protein and proteoglycan catabolism. These results support those reported by Kalbhen and Kalbert and are favouring the use of this drug in order to stimulate reparative processes of articular cartilage in osteoarthritis and aging.

Age-related changes in the synthesis of matrix macromolecules by bovine articular cartilage.

Calf and mature cow articular cartilage was labeled in vitro with [35S]SO4 and [3H]glycine and kinetics of incorporation of both isotopes by cartilage fragments was determined by scintillation spectroscopy. The cartilage fragments were then extracted in sequence with 4M GuHCl (Guanidium chloride) and pepsin. The pepsin digest was adjusted to 1.3 M NaCl and pepsin-solubilized collagen salted out. The 4M GuHCl extract, collagen and pepsin-resistent residue were then freeze-dried. The 4M GuHCl extract was further fractionated by DEAE (Diethylaminoethyl) 52 ion exchange chromatography to obtain protein and PG (Proteoglycan) fractions. The protein fraction was also characterised by SDS-PAGE and PG fraction by Sepharose C1-2B chromatography under associative conditions in the presence and absence of an exogenous HA (Hyaluronic acid). The GAG (Glycosaminoglycan) side chains of the PG samples were analysed by Sephadex G-200 column chromatography and their composition determined by paper chromatography after chondroitinase ABC digestion. Linear incorporation of both isotopes was observed from 1 to 18 hours of incubation and roughly equal amounts of [35S]SO4 counts were found on per cell bases in both cartilages although less [3H]glycine was incorporated by cow chondrocytes. It was also found that calf chondrocytes synthesize much greater proportion of the collagen whereas the cow cells synthesize PGs of smaller hydrodynamic sizes, bearing shorter GAG side chains that are enriched in KS (Keratan sulfate) and Ch-6S (Chondroitin-6 sulfate isomer). A failure of cow 35S-PGs monomers to interact with an exogenous HA in the presence of other extracted components was also demonstrated. The relevance of these findings for the mechanism of cartilage damage in aging and osteoarthritis is discussed.

Anti-inflammatory drugs, prostanoid and proteoglycan production by cultured bovine articular chondrocytes.

The effect of various anti-inflammatory drugs on the production of prostaglandins E2 and F2 alpha, 6 keto PGF1 alpha and thromboxane B2 by bovine articular chondrocytes was measured by radioimmunoassay. While indomethacin and meclofenamic acid caused a dose-dependent inhibition of all prostanoids measured, the effects of hydrocortisone and colchicine varied with respect to different prostanoids. Hydrocortisone (10(-7)M - 10(-13)M) both in the presence and absence of added arachidonic acid, resulted in an inhibition of prostaglandins E2 and F2 alpha, and to a lesser extent, 6 keto PGF 1 alpha, but TxB2 production was only slightly inhibited by the drug in the absence of arachidonic acid and markedly increased in its presence. Colchicine (10(-7)M-10(-3)M) had the opposite effect, causing an inhibition of TxB2 and stimulating PGE2 and 6 keto PGF1 alpha production. These findings suggest that certain anti-inflammatory drugs may, in addition to their action on phospholipase A2 and cyclo-oxygenases, exert potent effects at the level of the different synthetases. In order to see whether these alterations in relative prostanoid levels affected proteoglycan metabolism, the effect of anti-inflammatory drugs on proteoglycan synthesis by cultured chondrocytes was tested using 35SO4 labeling methodology. The results showed that at the concentrations tested (10(-5)M to 10(-7)M), indomethacin, dexamethasone, hydrocortisone and colchicine inhibited 35SO4 incorporation into newly synthesized proteoglycan molecules both in the presence (10(-6)M) and absence of exogenous arachidonic acid. In the same concentration range chloroquine had no effect. These results do not support the hypothesis of direct prostanoid involvement in the modulation of proteoglycan synthesis in articular cartilage.

Effects of various prostanoids on the in vitro metabolism of bovine articular chondrocytes.

The dose-dependent effects of 9 prostanoids (PGA1, PGA2, PGE1, PGE2, PGF1 alpha, PGF2 alpha, PGD2, PGI2, 6 keto-PGF1 alpha) on metabolism of cultured bovine articular chondrocytes were investigated. Most prostanoids dose-dependently inhibited 35SO4= and 3H-glycine incorporation. At 25 microgram/ml, the inhibitory sequence was A2 greater than or equal to D2 greater than E2= E1 = A1 greater than 6 keto-F1 alpha greater than F1 greater than F2, but sensitivity (lowest dose eliciting inhibition) followed the sequence E2 greater than 6 keto-F1 alpha = F1 greater than A2 = D2 greater than E1 greater than A1. At 25 microgram/ml, PGA2 also inhibited incorporation of 3H-cytidine and 3H-thymidine, but had no significant effect on 3H-glucose or 14C-xylose incorporation. The inhibitory effect of PGA2 was apparent after 30 minutes exposure for 35SO4= and after 60 minutes for 3H-cytidine, and was still present up to 72 hours following incubation in fresh non-PG-containing medium. PGI2 had no significant effect on 35SO4= incorporation but at concentrations below 10 microgram/ml enhanced uptake of 3H-glycine. The PG-induced inhibitory effect was apparently not due to cell damage as indicated by measurement of 3H-glucose metabolism and lactate production.

Metabolism of human femoral head cartilage in osteoarthrosis and subcapital fracture.

The cell density and incorporation of 35SO4 and 3H-glycine into human articular cartilage from 8 osteoarthrotic and 7 normal (subcapital fracture) femoral heads were studied. It was found that osteoarthrotic cartilage incorporates on a per cell basis about twice as much 35SO4 and 2--5 times as much 3H-glycine as normal cartilage. There was no relationship between the intensity of incorporation and either the location of the cartilage (weight-bearing versus non weight-bearing areas) in normal cartilage or the degree of damage (normal-like, fibrillated, and ulcerated) in osteoarthrotic articular cartilage. In the latter tissue the increased synthetic capacity of the cells seems to be a diffuse rather than a localised process, for it was also found in cartilage from peripheral osteophytes. Histo-autoradiographic studies showed that the osteoarthrotic chondrocytes are metabolically hyperactive all over the femoral head, including wedge-shaped margins of the zone of exposed bone. These results support the hypothesis that much of the articular cartilage from osteoarthrotic femoral heads is of an immature chondroblastic type. It is suggested that de-novo synthesis of articular cartilage occurs during the process of regional remodelling of the femoral head, which would account for the observed hyperactivity.