Structure and dynamics of the supercluster of galaxies SC0028-0005

According to the standard cosmological scenario, superclusters are objects that have just passed the turn around point and are collapsing. The dynamics of very few superclusters have been analysed up to now. In this paper we study the supercluster SC0028-0005, at redshift 0.22, identify the most prominent groups and/or clusters that make up the supercluster, and investigate the dynamic state of this structure. For the membership identification, we have used photometric and spectroscopic data from SDSS-DR10, finding 6 main structures in a flat spatial distribution. We have also used a deep multi-band observation with MegaCam/CFHT to estimate de mass distribution through the weak-lensing effect. For the dynamical analysis, we have determined the relative distances along the line of sight within the supercluster using the Fundamental Plane of early-type galaxies. Finally, we have computed the peculiar velocities of each of the main structures. The 3D distribution suggests that SC0028-005 is indeed a collapsing supercluster, supporting the formation scenario of these structures. Using the spherical collapse model, we estimate that the mass within $r = 10$~Mpc should lie between 4 and $16 \times 10^{15} M_\odot$. The farthest detected members of the supercluster suggest that within $\sim 60$~Mpc the density contrast is $\delta \sim 3$ with respect to the critical density at $z=0.22$, implying a total mass of $\sim 4.6$--$16 \times 10^{17} M_\odot$, most of which in the form of low-mass galaxy groups or smaller substructures.Comment: 12 pages, 9 figures, Accepted for publication in MNRA

Kinematic Self-Similarity

Self-similarity in general relativity is briefly reviewed and the differences between self-similarity of the first kind and generalized self-similarity are discussed. The covariant notion of a kinematic self-similarity in the context of relativistic fluid mechanics is defined. Various mathematical and physical properties of spacetimes admitting a kinematic self-similarity are discussed. The governing equations for perfect fluid cosmological models are introduced and a set of integrability conditions for the existence of a proper kinematic self-similarity in these models is derived. Exact solutions of the irrotational perfect fluid Einstein field equations admitting a kinematic self-similarity are then sought in a number of special cases, and it is found that; (1) in the geodesic case the 3-spaces orthogonal to the fluid velocity vector are necessarily Ricci-flat and (ii) in the further specialisation to dust the differential equation governing the expansion can be completely integrated and the asymptotic properties of these solutions can be determined, (iii) the solutions in the case of zero-expansion consist of a class of shear-free and static models and a class of stiff perfect fluid (and non-static) models, and (iv) solutions in which the kinematic self-similar vector is parallel to the fluid velocity vector are necessarily Friedmann-Robertson-Walker (FRW) models.Comment: 29 pages, AmsTe

Neurogenic inflammation after traumatic brain injury and its potentiation of classical inflammation

Background: The neuroinflammatory response following traumatic brain injury (TBI) is known to be a key secondary injury factor that can drive ongoing neuronal injury. Despite this, treatments that have targeted aspects of the inflammatory pathway have not shown significant efficacy in clinical trials. Main body: We suggest that this may be because classical inflammation only represents part of the story, with activation of neurogenic inflammation potentially one of the key initiating inflammatory events following TBI. Indeed, evidence suggests that the transient receptor potential cation channels (TRP channels), TRPV1 and TRPA1, are polymodal receptors that are activated by a variety of stimuli associated with TBI, including mechanical shear stress, leading to the release of neuropeptides such as substance P (SP). SP augments many aspects of the classical inflammatory response via activation of microglia and astrocytes, degranulation of mast cells, and promoting leukocyte migration. Furthermore, SP may initiate the earliest changes seen in blood-brain barrier (BBB) permeability, namely the increased transcellular transport of plasma proteins via activation of caveolae. This is in line with reports that alterations in transcellular transport are seen first following TBI, prior to decreases in expression of tight-junction proteins such as claudin-5 and occludin. Indeed, the receptor for SP, the tachykinin NK1 receptor, is found in caveolae and its activation following TBI may allow influx of albumin and other plasma proteins which directly augment the inflammatory response by activating astrocytes and microglia. Conclusions: As such, the neurogenic inflammatory response can exacerbate classical inflammation via a positive feedback loop, with classical inflammatory mediators such as bradykinin and prostaglandins then further stimulating TRP receptors. Accordingly, complete inhibition of neuroinflammation following TBI may require the inhibition of both classical and neurogenic inflammatory pathways.Frances Corrigan, Kimberley A. Mander, Anna V. Leonard and Robert Vin

On the nonlinear hunting stability of a high-speed train bogie

The hunting phenomenon is an intrinsic swaying motion appearing in railway vehicles due to the vehicle’s forward speed and the wheel–rail contact forces. Hunting motion consists of wheelset and other vehicle’s components oscillations that arise above a certain vehicle’s speed known as critical or hunting speed. These oscillations are of unstable nature and represent a safety hazard as they could lead to the vehicle’s derailment. This article analyses the stability of a bogie nonlinear model for a Spanish high-speed train when this is travelling at speeds near the hunting speed. The vehicle’s stability is studied by means of root loci methods, and the value of the critical speed is found. In addition to this, the behaviour of the vehicle is studied in both stable and unstable regions and the existence of limit cycles is discussed in this work. Finally, a sensitivity analysis of the axle load and suspension parameters is performed. The results show that the axle load, the vertical stiffness of the primary suspension and the lateral damping of the secondary suspension have a significant influence on the value of the critical speed

Clinical study of cervicogenic headache

The cervicogenic headache was studied to get a deeper insight into the pathogenetic mechanisms, and clinical presentation forms. Material and Methods. Eleven female patients, ranging from 34 to 81 years-old, with cervicogenic headaches, were studied and correlated with NMR images of the cervical spine. Results. Intense neck pain irradiated to parietal, occipital, temporal regions, and shoulders were correlated with NMR images of the degenerated cervical spine. Also, lumbar spine pathology, osteoporosis, gallstones, and cholecystitis were found. The following associated neurological, neurobehavioral, and metabolic diseases comorbidities were observed, such as blood hypertension, diabetes, obesity, hypothyroidism, partial epilepsy, tremor, familial stress, memory, sleep disorders, and dizziness. Also, we found mixed cervicogenic headaches and migraines in 50% of cases studied. Conclusion. The headache and the associated images of cervical pathology have been clinically interpreted as cardinal signs of cervicogenic headache. A mixed cervicogenic mixed type was observed

Zinc depletion regulates the processing and secretion of IL-1β.

Sterile inflammation contributes to many common and serious human diseases. The pro-inflammatory cytokine interleukin-1β (IL-1β) drives sterile inflammatory responses and is thus a very attractive therapeutic target. Activation of IL-1β in sterile diseases commonly requires an intracellular multi-protein complex called the NLRP3 (NACHT, LRR, and PYD domains-containing protein 3) inflammasome. A number of disease-associated danger molecules are known to activate the NLRP3 inflammasome. We show here that depletion of zinc from macrophages, a paradigm for zinc deficiency, also activates the NLRP3 inflammasome and induces IL-1β secretion. Our data suggest that zinc depletion damages the integrity of lysosomes and that this event is important for NLRP3 activation. These data provide new mechanistic insight to how zinc deficiency contributes to inflammation and further unravel the mechanisms of NLRP3 inflammasome activation

Sertoli cells have a functional NALP3 inflammasome that can modulate autophagy and cytokine production

Sertoli cells, can function as non-professional tolerogenic antigen-presenting cells, and sustain the blood-testis barrier formed by their tight junctions. The NOD-like receptor family members and the NALP3 inflammasome play a key role in pro-inflammatory innate immunity signalling pathways. Limited data exist on NOD1 and NOD2 expression in human and mouse Sertoli cells. Currently, there is no data on inflammasome expression or function in Sertoli cells. We found that in primary pre-pubertal Sertoli cells and in adult Sertoli line, TLR4\NOD1 and NOD2 crosstalk converged in NF?B activation and elicited a NALP3 activation, leading to de novo synthesis and inflammasome priming. This led to caspase-1 activation and IL-1? secretion. We demonstrated this process was controlled by mechanisms linked to autophagy. NOD1 promoted pro-IL-1? restriction and autophagosome maturation arrest, while NOD2 promoted caspase-1 activation, IL-1? secretion and autophagy maturation. NALP3 modulated NOD1 and pro-IL-1? expression, while NOD2 inversely promoted IL-1?. This study is proof of concept that Sertoli cells, upon specific stimulation, could participate in male infertility pathogenesis via inflammatory cytokine induction